At the end of each year, it is a useful practise to review the triumphs (and failures) of the past 12 months. It is an exercise of putting everything into perspective.
2017 has been an incredible year for Parkinson’s research.
And while I appreciate that statements like that will not bring much comfort to those living with the condition, it is still important to consider and appreciate what has been achieved over the last 12 months.
In this post, we will try to provide a summary of the Parkinson’s-related research that has taken place in 2017 (Be warned: this is a VERY long post!)
The number of research reports and clinical trial studies per year since 1817
As everyone in the Parkinson’s community is aware, in 2017 we were observing the 200th anniversary of the first description of the condition by James Parkinson (1817). But what a lot of people fail to appreciate is how little research was actually done on the condition during the first 180 years of that period.
The graphs above highlight the number of Parkinson’s-related research reports published (top graph) and the number of clinical study reports published (bottom graph) during each of the last 200 years (according to the online research search engine Pubmed – as determined by searching for the term “Parkinson’s“).
PLEASE NOTE, however, that of the approximately 97,000 “Parkinson’s“-related research reports published during the last 200 years, just under 74,000 of them have been published in the last 20 years.
That means that 3/4 of all the published research on Parkinson’s has been conducted in just the last 2 decades.
And a huge chunk of that (almost 10% – 7321 publications) has been done in 2017 only.
So what happened in 2017? Continue reading
On the 27th June, 1997, a research report was published in the prestigious scientific journal ‘Science’ that would change the world of Parkinson’s disease research forever.
And I am not exaggerating here.
The discovery that genetic variations in a gene called alpha synuclein could increase the risk of developing Parkinson’s disease opened up whole new areas of research and eventually led to ongoing clinical trials of potential therapeutic applications.
Todays post recounts the events surrounding the discovery, what has happened since, and we will discuss where things are heading in the future.
It is fair to say that 1997 was an eventful year.
In world events, President Bill Clinton was entering his second term, Madeleine Albright became the first female Secretary of State for the USA, Tony Blair became the prime minister of the UK, and Great Britain handed back Hong Kong to China.
#42 – Bill Clinton. Source: Wikipedia
In the world of entertainment, author J. K. Rowling’s debut novel “Harry Potter and the Philosopher’s Stone” was published by Bloomsbury, and Teletubbies, South Park, Ally McBeal, and Cold Feet (it’s a British thing) all appeared on TV for the first time, amusing and entertaining the various age groups associated with them.
South Park. Source: Hollywoodreporter
Musically, rock band Blur released their popular hit song ‘Song 2‘ (released 7th April), “Bitter Sweet Symphony” by the Verve entered the UK charts at number 2 in June, and rapper Notorious B.I.G. was killed in a drive by shooting. Oh, and let’s not forget that “Tubthumping” (also known as “I Get Knocked Down”) by Chumbawamba was driving everybody nuts for its ubiquitous presence.
And at the cinemas, no one seemed to care about anything except a silly movie called Titanic.
Titanic. Source: Hotspot
Feeling old yet?
In her excellent book – ‘The Enlightened Mr. Parkinson: The Pioneering Life of a Forgotten English Surgeon’ (Icon Books Ltd) – Dr Cherry Lewis wrote that the earliest reference to Mr James Parkinson’s ‘An Essay on the Shaking Palsy’ was an advert placed in the Morning Chronicle of Saturday 31st May (1817), under a list of books “published this day”.
Given this information, we searched the Britishnewspaperarchive online and captured the image presented above.
Today is the 200th anniversary of the publication of ‘An Essay on the Shaking Palsy’.
In this post, we continue our four part series on the man behind the disease by discussing the ‘Essay’ on the 200th anniversary of its publication.
The opening of Waterloo Bridge on the 18th of June 1817. Source: Thames
A few weeks before the opening of the Waterloo Bridge, James Parkinson published the booklet that would go on to immortalise him in the annals of medicine. An Essay on the Shaking Palsy, which spans 66 pages, was published by Sherwood, Neely and Jones of London, and printed by Whittingham and Rowland in 1817.
At the date of printing it sold for 3 shillings (approx. £9 or US$12).
Much has been written about the essay, and we here at the SoPD feel that we have little to actually add to the conversation. Thus our post today will simply provide an overview of the book (a highlights package, if you will), summarising it for those who do not have time to read its entirety (a full copy of the essay can be found by clicking here).
Source: Project Gutenberg
The Essay begins with a preface and is then divided into five chapters, labeled:
1. “DEFINITION—HISTORY—ILLUSTRATIVE CASES”
2. “PATHOGNOMONIC SYMPTOMS EXAMINED—TREMOR COACTUS—SCELOTYRBE FESTINANS”
3. “SHAKING PALSY DISTINGUISHED FROM OTHER DISEASES FROM WHICH IT MAY BE CONFOUNDED”
4. “PROXIMATE CAUSE—REMOTE CAUSES—ILLUSTRATIVE CASES”
5. “CONSIDERATIONS RESPECTING THE MEANS OF CURE”
In the preface of the book, James gave his reasons for actually writing it. Basically, he wanted to make others aware of what he considered a previously un-described condition.
At the heart of the preface is a paragraph, which reads:
“The disease is of long duration: to connect, therefore, the symptoms which occur in its later stages with those which mark its commencement, requires a continuance of observation of the same case, or at least a correct history of its symptoms, even for several years. Of both these advantages the writer has had the opportunities of availing himself; and has hence been led particularly to observe several other cases in which the disease existed in different stages of its progress. By these repeated observations, he hoped that he had been led to a probable conjecture as to the nature of the malady, and that analogy had suggested such means as might be productive of relief, and perhaps even of cure, if employed before the disease had been too long established. He therefore considered it to be a duty to submit his opinions to the examination of others, even in their present state of immaturity and imperfection.”
At the end of the preface, James hopes that “friends to humanity and medical science…might be excited to extend their researches to this malady”. And in that situation James would “think himself fully rewarded by having excited the attention of those, who may point out the most appropriate means of relieving a tedious and most distressing malady”.
In the first chapter, James begins with a description of the Shaking Palsy (or ‘Paralysis agitans’ as he called it), that resembles modern Parkinson’s disease almost perfectly:
“Involuntary tremulous motion, with lessened muscular power, in parts not in action and even when supported; with a propensity to bend the trunk forwards, and to pass from a walking to a running pace: the senses and intellects being uninjured.”
He then moves on to provide a breakdown of the features that make up this condition, which includes a history of tremor that takes into account the works of Aelius “Galen” Galenus, Sylvius de la Boë, and Johann Juncker.
James starts by noting the slow progress of the condition:
“So slight and nearly imperceptible are the first inroads of this malady, and so extremely slow is its progress, that it rarely happens, that the patient can form any recollection of the precise period of its commencement. The first symptoms perceived are, a slight sense of weakness, with a proneness to trembling in some particular part; sometimes in the head, but most commonly in one of the hands and arms.”
How familiar does this sound?
And please remember, James was describing this condition for the first time based only on his own observations of just six individuals (three from a distance). His attention to detail was amazing, taking into account so many different aspects of the condition (from the obvious motor features to issues with bowel movements). And he noted it all down in the essay.
He continues by describing the progress of the condition over time:
“But as the malady proceeds,….The propensity to lean forward becomes invincible, and the patient is thereby forced to step on the toes and fore part of the feet, whilst the upper part of the body is thrown so far forward as to render it difficult to avoid falling on the face.”
His description took into account the entire history of the condition, starting from the appearance of the first features and finishing with the late stages of the disease:
“As the disease proceeds towards its last stage, the trunk is almost permanently bowed, the muscular power is more decidedly diminished, and the tremulous agitation becomes violent….As the debility increases and the influence of the will over the muscles fades away, the tremulous agitation becomes more vehement. It now seldom leaves him for a moment;”
After describing the basic clinical appearance of the condition, James then immediately moves on to each of the six cases he based his description on.
Case I was the first encounter of this condition for James. It was also probably one of the case that James was most familiar with as he wrote “every circumstance occurred which has been mentioned in the preceding history”. In his writing of Case I, however, James was rather brief:
“The subject of this case was a man rather more than fifty years of age, who had industriously followed the business of a gardener, leading a life of remarkable temperance and sobriety. The commencement of the malady was first manifested by a slight trembling of the left hand and arm, a circumstance which he was disposed to attribute to his having been engaged for several days in a kind of employment requiring considerable exertion of that limb. Although repeatedly questioned, he could recollect no other circumstance which he could consider as having been likely to have occasioned his malady.”
The “next case” (as James wrote it, indicating that the cases are presented in chronological order), Case II, was a man that James casually met with in the street.
“It was a man sixty-two years of age; the greater part of whose life had been spent as an attendant at a magistrate’s office. He had suffered from the disease about eight or ten years. All the extremities were considerably agitated, the speech was very much interrupted, and the body much bowed and shaken. He walked almost entirely on the fore part of his feet, and would have fallen every step if he had not been supported by his stick. He described the disease as having come on very gradually,…”
Case II attributed his condition to his choice of lifestyle (“irregularities in mode of living and indulgence in spiritous liquors,”), which James did not give any credit. This was probably because much of the rest of the city partook in such a lifestyle without the emergence of the disease. Ever the humanitarian, though, James points towards the unfortunate situation that these individuals found themselves:
“He was the inmate of a poor-house of a distant parish, and being fully assured of the incurable nature of his complaint, declined making any attempts for relief.”
The third case was also “noticed casually in the street“. James did interact with the man though, determining that he had been a sailor who attributed his condition to having been for many months in a Spanish prison:
“The subject…was a man of about sixty-five years of age, of a remarkable athletic frame. The agitation of the limbs, and indeed of the head and of the whole body, was too vehement to allow it to be designated as trembling. He was entirely unable to walk; the body being so bowed, and the head thrown so forward, as to oblige him to go on a continued run, and to employ his stick every five or six steps to force him more into an upright posture, by projecting the point of it with great force against the pavement.”
The 4th case was a gentleman (of about fifty-five years of age) who presented himself to James. He claimed that he had first experienced the trembling of the arms about five years before. In this case, we see the nature of the medical treatments during that period (that being a preference for blood letting):
“His application was on account of a considerable degree of inflammation over the lower ribs on the left side, which terminated in the formation of matter beneath the fascia. About a pint was removed on making the necessary opening; and a considerable quantity discharged daily for two or three weeks. On his recovery from this, no change appeared to have taken place in his original complaint; and the opportunity of learning its future progress was lost by his removal to a distant part of the country”
Case V was the subject that James had the least amount of information about and observed the gentleman only from a distance (it is curious to note that all of these cases were males – who have a higher risk of developing Parkinson’s disease – click here for more on this):
“…one of the characteristic symptoms of this malady, the inability for motion, except in a running pace, appeared to exist in an extraordinary degree. It seemed to be necessary that the gentleman should be supported by his attendant, standing before him with a hand placed on each shoulder, until, by gently swaying backward and forward, he had placed himself in equipoise; when, giving the word, he would start in a running pace, the attendant sliding from before him and running forward, being ready to receive him and prevent his falling, after his having run about twenty paces”
Case VI may have been the individual that spurred James to write his essay as it was one “which presented itself to observation since those above-mentioned,”. Thus, James had the benefit of hindsight and all the information that he had gained from the previous cases, when he was confronted with Case VI and he could make a thorough study of the individual. In case VI, James also hints at the indiscriminate nature of the condition, afflicting people from all sorts of backgrounds.
“The gentleman who was the subject of it is seventy-two years of age. He has led a life of temperance, and has never been exposed to any particular situation or circumstance which he can conceive likely to have occasioned, or disposed to this complaint; which he rather seems to regard as incidental upon his advanced age, than as an object of medical attention….About eleven or twelve, or perhaps more, years ago, he first perceived weakness in the left hand and arm, and soon after found the trembling commence. In about three years afterwards the right arm became affected in a similar manner: and soon afterwards the convulsive motions affected the whole body, and began to interrupt the speech…Of late years the action of the bowels had been very much retarded;…”
James notes with Case VI that the gentleman had the capacity to temporarily control his situation by his own will:
“…he, being then just come in from a walk, with every limb shaking, threw himself rather violently into a chair, and said, ‘Now I am as well as ever I was in my life.’ The shaking completely stopped; but returned within two minutes”
At the end of the section on CaseVI, James notes some input from the wife of the gentleman:
“…if whilst walking he felt much apprehension from the difficulty of raising his feet, if he saw a rising pebble in his path? he avowed, in a strong manner, his alarm on such occasions; and it was observed by his wife, that she believed, that in walking across the room, he would consider as a difficulty the having to step over a pin”
Having finished reading Chapter 1, it is truly remarkable to recall that James was describing what he thought was a previously unrecognised condition. Remarkable because of the depth and scope he provides. It is difficult to put oneself in his shoes, given that we are now so familiar with the disease. But it does Mr Parkinson great credit both as a surgeon and a writer that what he is describing feels so familiar.
Here James returns to the cardinal features of the condition as he sees them, starting with the tremor:
1. Involuntary tremulous motion, with lessened voluntary muscular power, in parts, not in action, and even supported.
In this first section, James breaks down the different types of tremor in an effort to better understand this condition he is describing.
“It is necessary that the peculiar nature of this tremulous motion should be ascertained, as well for the sake of giving to it its proper designation, as for assisting in forming probable conjectures, as to the nature of the malady, which it helps to characterise”
Galen. Source: thefamouspeople
“The separation of palpitation of the limbs (Palmos of Galen, Tremor Coactus of de la Boë) from tremor, is the more necessary to be insisted on, since the distinction may assist in leading to a knowledge of the seat of the disease.”
de la Boë. Source: Wikipedia
James concludes that the tremor associated with his new condition is distinct given that the tremor is nearly constant or “induced immediately on bringing the parts into action”
The second characteristic feature of this newly described condition, according to James, is the gait and posture:
2. A propensity to bend the trunk forwards, and to pass from a walking to a running pace.
Here James discusses the works of François Boissier de Sauvages de Lacroix (1706 – 1767), a French physician and botanist who is credited with establishing a methodical nosology for diseases (a classification system).
de Sauvage. Source: Homeoint
“Mons. de Sauvages attributes this complaint to a want of flexibility in the muscular fibres. Hence, he supposes, that the patients make shorter steps, and strive with a more than common exertion or impetus to overcome the resistance; walking with a quick and hastened step, as if hurried along against their will”
It is a demonstration of Mr Parkinson’s studious nature and high general level of intelligence that he was so familiar with the works of de Sauvage – it is a simple task for us modern folk to simply ‘google’ anything we don’t know or are curious about. Where did James go to find his background research for his Esssay?
Having clearly outlined the features of the condition, James next moves to Chapter 3 where he attempts to differentiate this condition from other maladies.
James did not want to have this new condition he was describing confused with other diseases, hence the meticulous description of the symptoms/features.
“…it is necessary to show that it is a disease which does not accord with any which are marked in the systematic arrangements of nosologists; and that the name by which it is here distinguished has been hitherto vaguely applied to diseases very different from each other, as well as from that to which it is now appropriated”
James’ choice of name for the new condition was ‘Shaking palsy’, but he noted that this label had been used several times before. For example, one Dr. Charlton had used the label in describing a particular case:
“Another case, which the Doctor designates as ‘A Shaking Palsy,’ apparently from worms, he describes thus, “A poor boy, about twelve or thirteen years of age, was seized with a Shaking Palsy. His legs became useless, and together with his head and hands, were in continual agitation; after many weeks trial of various remedies, my assistance was desired…His bowels being cleared, I ordered him a grain of Opium a day in the gum pill; and in three or four days the shaking had nearly left him.” By pursuing this plan, the medicine proving a vermifuge, he could soon walk, and was restored to perfect health”
Given the level of detail that James goes into in other chapters, it is fair to say that chapter 3 is light reading. But it finishes strong as James describes the truly distinguishing feature of his version of Shaking palsy – that being the resting state nature of the tremor:
“If the trembling limb be supported, and none of its muscles be called into action, the trembling will cease. In the real Shaking Palsy the reverse of this takes place, the agitation continues in full force whilst the limb is at rest and unemployed;”
And it was this feature for James that could be used to distinguish it from other conditions.
In Chapter 4, James tries to understand the cause of the condition, but right up front he acknowledges that this is a rather difficult task:
“Unaided by previous inquiries immediately directed to this disease, and not having had the advantage, in a single case, of that light which anatomical examination yields, opinions and not facts can only be offered”
In addition, James notes that “Cases illustrative of the nature and cause of this malady are very rare”
He does an admirable job in his endeavour here, however, by looking at previously reported cases of other diseases that share some similarities with this new condition. And James actually describes cases that he himself has dealt with (albeit by informally), but he takes pains to point out that these cases are different to the new conditions that he is describing in this essay. For example:
“…the unhappy subject of this malady was casually met in the street, shifting himself along, seated in a chair; the convulsive motions having ceased, and the limbs having become totally inert, and insensible to any impulse of the will”
In this case, the man had been treated with mercury for a venereal infection (click here to read more about early mercury treatments) many years before, which had left him with convulsive movements restricted to the legs.
Using this case study approach, however, James proposes that the disease is targeting or affecting an area of the brain stem called the medulla oblongata (which is affected in Parkinson’s disease, and is actually not too far from the midbrain where the significant loss of the dopamine neurons gives rise to the motor features of Parkinson’s disease).
Location of the midbrain and medulla in the human brain. Source: Wikipedia
In chapter 5, James expresses hope that a successful treatment is almost at hand:
“…there appears to be sufficient reason for hoping that some remedial process may ere long be discovered, by which, at least, the progress of the disease may be stopped”
Exactly 200 years on, I think it is fair to say that James was a bit too optimistic in nature, but we are certainly a lot closer now to stopping the disease than he was then.
James was instructive in how he thought it was best to attack the condition. He divides the condition into two halves, early and late, based on the spread of the motor features from individual limbs to other areas of the body. And he is rather certain that early diagnosis was essential if there was to be any chance of cure.
He also thought that the condition simply required some reverse engineering:
“…it seems as if we were able to trace the order and mode in which the morbid changes may proceed in this disease”
But his thoughts on how to treat the disease were largely based on the medical practises of the time (as they are today):
“…blood should be first taken from the upper part of the neck,…After which vesicatories should be applied to the same part, and a purulent discharge obtained by appropriate use of the Sabine Liniment; having recourse to the application of a fresh blister, when from the diminution of the discharging surface, pus is not secreted in a sufficient quantity”
He provides further thoughts on this treatment, but then offers the caveat that this is merely an opinion:
“Until we are better informed respecting the nature of this disease, the employment of internal medicines is scarcely warrantable;”
James also then comments on the insidious nature and the slow progress of the disease, as it:
“Seldom occurring before the age of fifty, and frequently yielding but little inconvenience for several months, it is generally considered as the irremediable diminution of the nervous influence, naturally resulting from declining life; and remedies therefore are seldom sought for”
And this leaves the sufferer focusing on:
“The weakened powers of the muscles in the affected parts is so prominent a symptom, as to be very liable to mislead the inattentive, who may regard the disease as a mere consequence of constitutional debility. If this notion be pursued, and tonic medicines, and highly nutritious diet be directed, no benefit is likely to be thus obtained; since the disease depends not on general weakness, but merely on the interruption of the flow of the nervous influence to the affected parts”
This is very insightful of James. He understood that it was not the weakness felt in the muscles that was paramount in this condition, but rather a dysfunction in the brain.
He concludes the essay with the following:
“To such researches the healing art is already much indebted for the enlargement of its powers of lessening the evils of suffering humanity. Little is the public aware of the obligations it owes to those who, led by professional ardour, and the dictates of duty, have devoted themselves to these pursuits, under circumstances most unpleasant and forbidding. Every person of consideration and feeling, may judge of the advantages yielded by the philanthropic exertions of a Howard; but how few can estimate the benefits bestowed on mankind, by the labours of a Morgagni, Hunter, or Baillie.
Regarding the last line, I may be displaying my ignorance here with regards to ‘a Howard’, but I suspect James is referring to John Howard (1726 – 1790), an English philanthropist of James’ era:
John Howard. Source: Wikipedia
Although, “a Howard” is also an old slang term used to describe a man (any man) of great character!
Giovanni Battista Morgagni. Source: Wikipedia
Giovanni Battista Morgagni (1682 – 1771) was an Italian anatomist, who is generally regarded as the father of modern anatomical pathology.
John Hunter. Source: Wikipedia
John Hunter (1728 – 1793) was a Scottish surgeon – one of the most distinguished scientists/surgeons of his day. He was an early advocate of careful observation and scientific method in medicine, and James personally learned a great deal from him. Between October 1785 and April 1786, James attended the evening lectures provided by Hunter. James wrote down the lectures verbatim (in shorthand) and his notes were later published by his son John (“Hunterian Reminiscences, Being The Substance Of A Course Of Lectures On The Principles And Practice Of Surgery Delivered By John Hunter In The Year 1785″ – a precious resource given that Hunter’s own notes were later destroyed by fire).
Matthew Baillie. Source: Wikipedia
Matthew Baillie was another Scottish physician and pathologist. A pupil of his uncle, John Hunter (above), Ballie provided us with the first systematic study of pathology. James was certainly familiar with Ballie, as he cited his works.
For further reading on An Essay on the Shaking Palsy we recommend a review written by Prof Brian Hurwitz (King’s College London) called Urban Observation and Sentiment in James Parkinson’s Essay on the Shaking Palsy (1817) which provides fantastic insight into James, the age he lived in, the essay itself, and the reception of the essay (Click here to read that review).
This post was written in observation of the 200 year anniversary of the publishing of the Essay on the Shaking Palsy. It is part two in a four part series on the life of Mr James Parkinson (click here for part one). In the third instalment, we will look at his life’s work, before the fourth part looks at his final years and his legacy.
The banner for today’s post was sourced from the Britishnewspaperarchive
Here at the SoPD we understand and are deeply sympathetic to the frustration felt by the Parkinson’s community regarding the idea of ‘200 years and still no cure’.
As research scientists, we are in the trench everyday – fighting the good fight – trying to find ways of alleviating this terrible condition. And some of us are also in the clinics, interacting with sufferers and their families, listening to their stories and trying to help. While we do not deal directly with the day-to-day trials of living with Parkinson’s disease, we are keenly aware of many of the issues and are fully invested in trying to correct this condition.
We do feel, however, that it is important to put some context into that ‘200 years’ time point that we are observing this week. It is too easy for people to think “wow, 200 years and still no cure?”
In our previous post – made in collaboration with Prof Frank Church of the Journey with Parkinson’s blog – we listed the major historical milestones and discoveries made in the Parkinson’s disease field during the last 200 years.
The most striking feature of that time line, however, is how just little actually happened during the first 100 years.
In fact for most of that period, Parkinson’s disease wasn’t even called ‘Parkinson’s disease’.
Of the 48 events that we covered on that time line, 37 of them have occurred in the last 50 years (26 since 2000).
Taking this line of thought one step further, 2017 is also the 20 year anniversary of the discovery of alpha synuclein‘s association with Parkinson’s disease. And what a remarkable 20 years that has been. In 1997, a group of researcher at the National institute of Health led by Robert Nussbaum reported the first genetic mutation in the alpha synuclein gene that infers vulnerability to Parkinson’s disease.
Since then, we have:
- identified multiple additional mutations within that same gene that increase the risk of developing Parkinson’s disease.
- determined which forms of alpha synuclein are toxic.
- identified alpha synuclein as an important component of Lewy bodies – the dense clusters of protein found in the Parkinsonian brain.
- discovered numerous methods by which alpha synuclein can be passed between cells – potentially aiding in the spread of Parkinson’s disease.
- developed and validated models of Parkinson’s disease based on manipulations of alpha synuclein (including numerous genetically engineered mice, viral over-expression models, etc).
- identified alpha synuclein in the lining of the gut of people with Parkinson’s disease and this has aided us in developing new theories as to how the condition may start.
- set up and run numerous clinical trials targeting alpha synuclein (and we eagerly await the results of those trials).
- published over 6200 scientific papers (don’t believe me? Click here) – that’s over 300 publications per year!
Alpha synuclein protein. Source: Wikipedia
And the truly amazing part? All of these particular achievements are only dealing with just the one gene: alpha synuclein.
Since the identification of the alpha synuclein mutations, we have subsequently discovered genetic mutations in over 20 other genes that increase the risk of developing Parkinson’s disease. And we have conducted the same activities/experiments for most of those genes as we have for alpha synuclein.
For example, in 2004 we discovered that people with genetic mutations in a gene called glucocerebrosidase (or GBA) had an increased risk of developing Parkinson’s disease. In 2016, just 12 years after that discovery we have started a clinical trial designed specifically for those people (Click here for more on this).
Source: Parkinson’s UK
We here at the SoPD are fully supportive of campaigns like #WeWontWait, and this post was not written (nor meant to be taken) as an excuse response to the ‘200 years and no cure’ frustration. I can understand how it may be read that way, but I did not know how else to write it. And I thought it needed to be written.
The point of this entire post is that those 200 years need to be put into context.
And while all of these words aren’t going to make life easier for someone living with Parkinson’s to deal with their situation, in addition to raising awareness this week I think it is important for the Parkinson’s community to also understand just how far we have come, and how fast we are currently progressing.
The question can be asked: will this be the last major anniversary we acknowledge with regards to Parkinson’s disease?
I sincerely think that there is cause to hope that it is.
Let me finish with a personal note:
I have a good friend – let’s call him Matt.
As a young boy, Matt remembers his grandfather having Parkinson’s disease. He remembers growing up watching the trials and tribulations that the old man went through with the condition. There were basically no treatment options when Matt’s grandfather was diagnosed and little in the way of support for the family. His grandfather’s body simply froze up as the disease progressed. L-dopa probably only became available to Matt’s grandfather during the latter stages of the disease.
Four years ago Matt’s father was diagnosed with Parkinson’s disease.
Thanks to scientific advances, however, Matt’s dad now has a wide range of treatment options on the medication side of things. The disease can be managed so that he can still play his golf and enjoy his retirement – in a way that his own father never could. He also has numerous surgical options once those medications lose their effectiveness (eg. deep brain stimulation, Pallidotomy, etc). The chances are very likely that Matt’s father will pass on by natural causes before he requires many of those additional options.
This is the progress that we have made.
But there is still a lot of work to be done of course.
During a lunch shortly after his father’s diagnosis, Matt looked squarely across the table at me. Me, the Parkinson’s researcher. All of the usual jovial nature was missing from his face and he simply muttered the words ‘hurry up’.
Whether he was speaking for his father, himself or his own young kids, I understood where his words were coming from and the sentiment.
And, as this post and the previous post point out, we are hurrying up.
The banner for today’s post was sourced from BMO
For today’s post, we have teamed up with Prof Frank Church from the Journey with Parkinson’s blog to bring readers an ‘Introduction to the historical timeline on Parkinson’s disease’.
The idea for this project started as a conversation between Frank and his partner Barbara during a recent weekend at the beach in North Carolina.
Frank said: “Wouldn’t it be cool to publish a Parkinson’s historical timeline for Parkinson’s awareness month?”
However, to complete this project Frank felt it necessary to bring in some extra help in the form of a Parkinson’s expert.
And when everyone else said they were too busy, Frank contacted us.
Truly flattered, we immediately said yes. And the rest is history.
We are happy to present the milestones in Parkinson’s disease research and discover, though we do apologise to the clinicians, scientists, health-care specialists, and their projects that were not cited here but we limited the timeline to ~50 notations.
Below there are six panels outlining different stages of the history of Parkinson’s disease, and under each of them we have briefly described each of the events in the panel.
We hope you like it.
1817-1919- Milestones in Parkinson’s Disease Research and Discovery (Part 1a: Historical):
First description of Parkinson’s disease
In 1811, Mr James Parkinson of no. 1 Hoxton Square (London) published a 66 page booklet called an ‘An Essay on the Shaking Palsy’. At the date of printing, it sold for 3 shillings (approx. £9 or US$12). The booklet was the first complete description of a condition that James called ‘Paralysis agitans’ or shaking palsy. In his booklet, he discusses the history of tremor and distinguishes this new condition from other diseases. He then describes three of his own patients and three people who he saw in the street.
The naming of Parkinson’s disease
Widely considered the ‘Father of modern neurology’, the importance of Jean-Martin Charcot’s contribution to modern medicine is rarely in doubt. From Sigmund Freud to William James (one of the founding fathers of Psychology), Charcot taught many of the great names in the early field of neurology. Between 1868 and 1881, Charcot focused much of his attention on the ‘paralysis agitans’. Charcot rejected the label ‘Paralysis agitans’, however, suggesting that it was misleading in that patients were not markedly weak and do not necessarily have tremor. Rather than Paralysis Agitans, Charcot suggested that Maladie de Parkinson (or Parkinson’s disease) would be a more appropriate name, bestowing credit to the man who first described the condition. And thus 70 years after passing away, James Parkinson was immortalized with the disease named after him.
The further clinical characterisation of Parkinson’s disease
British neurologist Sir William Gowers published a two-volume text called the Manual of Diseases of the Nervous System (1886, 1888). In this book he described his personal experience with 80 people with Parkinson’s disease in the 1880s. He also identified the subtle male predominance of the disorder and provided illustrations of the characteristic posture. In his treatment of Parkinson’s tremor, Gower used hyoscyamine, hemlock, and hemp (cannabis) as effective agents for temporary tremor abatement.
The discovery of the chemical dopamine
In the Parkinsonian brain there is a severe reduction in the chemical dopamine. This chemical was first synthesised in 1910 by George Barger and James Ewens at the Wellcome labs in London, England.
The discovery of Lewy bodies
One of the cardinal features of Parkinson’s disease in the brain is the presence of Lewy bodies – circular clusters of protein. In 1912, German neurologist Friedrich Lewy, just two years out of medical school and still in his first year as Director of the Neuropsychiatric Laboratory at the University of Breslau (now Wroclaw, Poland) Medical School discovered these ‘spherical inclusions’ in the brains of a people who had died with Parkinson’s disease.
The importance of the substantia nigra in Parkinson’s disease
The first brain structure to be associated with Parkinson’s disease was the substantia nigra. This region lies in an area called the midbrain and contains the majority of the dopamine neurons in the human brain. It was in 1919 that a Russian graduate student working in Paris, named Konstantin Tretiakoff, first demonstrated that the substantia nigra was associated with Parkinson’s disease. Tretiakoff also noticed circular clusters in the brains he examined and named them ‘corps de Lewy’ (or Lewy bodies) after the German neurologist Friedrich Lewy who first discovered them.
1953-1968- Milestones in Parkinson’s Disease Research and Discovery (Part 1b: Historical):
The first complete pathologic analysis of the Parkinsonian brain
The most complete pathologic analysis of Parkinson’s disease with a description of the main sites of damage was performed in 1953 by Joseph Godwin Greenfield and Frances Bosanquet.
The discovery of a functional role for dopamine in the brain
Until the late 1950s, the chemical dopamine was widely considered an intermediate in the production of another chemical called norepinephrine. That is to say, it had no function and was simply an ingredient in the recipe for norepinephrine. Then in 1958, Swedish scientist Arvid Carlsson discovered that dopamine acts as a neurotransmitter – a discovery that won Carlsson the 2000 Nobel prize for Physiology or Medicine.
The founding of the Parkinson’s Disease Foundation
In 1957, a nonprofit organisation called the Parkinson’s Disease Foundation was founded by William Black. It was committed to finding a cure for Parkinson’s Disease. Since its founding in 1957, PDF has funded more than $115 million worth of scientific research in Parkinson’s disease.
The discovery of the loss of dopamine in the brain of people with Parkinson’s disease
In 1960, Herbert Ehringer and Oleh Hornykiewicz demonstrated that the chemical dopamine was severely reduced in brains of people who had died with Parkinson’s disease.
The first clinical trials of Levodopa
Knowing that dopamine can not enter the brain and armed with the knowledge that the chemical L-dopa was the natural ingredient in the production of dopamine, Oleh Hornykiewicz & Walther Birkmayer began injecting people with Parkinson’s disease with L-dopa in 1961. The short term response to the drug was dramatic: “Bed-ridden patients who were unable to sit up, patients who could not stand up when seated, and patients who when standing could not start walking performed all these activities with ease after L-dopa. They walked around with normal associated movements and they could even run and jump.” (Birkmayer and Hornykiewicz 1961).
The first internationally-used rating system for Parkinson’s disease
In 1967, Melvin Yahr and Margaret Hoehn published a rating system for Parkinson’s disease in the journal Neurology. It involves 5 stages, ranging from unilateral symptoms but no functional disability (stage 1) to confinement to wheel chair (stage 5). Since then, a modified Hoehn and Yahr scale has been proposed with the addition of stages 1.5 and 2.5 in order to help better describe the intermediate periods of the disease.
Perfecting the use of L-dopa as a treatment for Parkinson’s disease
In 1968, Greek-American scientist George Cotzias reported dramatic effects on people with Parkinson’s disease using oral L-dopa. The results were published in the New England Journal of Medicine. and L-dopa becomes a therapeutic reality with the Food and Drug Administration (FDA) approving the drug for use in Parkinson’s disease in 1970. Cotzias and his colleagues were also the first to describe L-dopa–induced dyskinesias.
1972-1997- Milestones in Parkinson’s Disease Research and Discovery (Part 1c: Historical):
Levodopa + AADC inhibitors (carbidopa or benserazide)
When given alone levodopa is broken down to dopamine in the bloodstream, which leads to some detrimental side effects. By including an aromatic amino acid decarboxylase (AADC) inhibitor with levodopa allows the levodopa to get to the blood-brain barrier in greater amounts for better utilisation by the neurons. In the U.S., the AADC inhibitor of choice is carbidopa and in other countries it’s benserazide.
The discovery of dopamine agonists
Dopamine agonists are ‘mimics’ of dopamine that pass through the blood brain barrier to interact with target dopamine receptors. Since the mid-1970’s, dopamine agonists are often the first medication given most people to treat their Parkinson’s; furthermore, they can be used in conjunction with levodopa/carbidopa. The most commonly prescribed dopamine agonists in the U.S. are Ropinirole (Requip®), Pramipexole (Mirapex®), and Rotigotine (Neupro® patch). There are some challenging side effects of dopamine agonists including compulsive behaviour (e.g., gambling and hypersexuality), orthostatic hypotension, and hallucination.
The clinical use of MAO-B inhibitors
In the late-1970’s, monoamine oxidase-B (MAO-B) inhibitors were created to block an enzyme in the brain that breaks down levodopa. MAO-B inhibitors have a modest effect in suppressing the symptoms of Parkinson’s. Thus, one of the functions of MAO-B inhibitors is to prolong the half-life of levodopa to facilitate its use in the brain. Very recently in clinical trials, it’s been shown that MAO-B inhibitors have some neuroprotective effect when used long-term. The most widely used MAO-B inhibitors in the U.S. include Rasagiline (Azilect) and Selegiline (Eldepryl and Zelpar); MAO-B inhibitors may reduce “off” time and extend “on” time of levodopa.
Fetal Cell transplantation
After successful preclinical experiments in rodents, a team of researchers in Sweden, led by Anders Bjorklund and Olle Lindvall, began the first clinical trials of fetal cell transplantation for Parkinson’s disease. These studies involved taking embryonic dopamine cells and injecting them into the brains of people with Parkinson’s disease. The cells then matured and replaced the cells that had been lost during the progression of the disease.
The discovery of MPTP
In July of 1982, Dr. J. William Langston of the Santa Clara Valley Medical Center in San Jose (California) was confronted with a group of heroin addicts who were completely immobile. A quick investigation demonstrated that the ‘frozen addicts’ had injected themselves with a synthetic heroin that had not been prepared correctly. The heroin contained a chemical called MPTP, which when injected into the body rapidly kills dopamine cells. This discovery provided the research community with a new tool for modelling Parkinson’s disease.
1997-2006- Milestones in Parkinson’s Disease Research and Discovery (Part 1d: Historical):
Alpha synuclein becomes the first gene associated with familial cases of Parkinson’s disease and its protein is found in Lewy bodies
In 1997, a group of researchers at the National institute of Health led by Robert Nussbaum reported the first genetic aberration linked to Parkinson’s disease. They had analysed DNA from a large Italian family and some Greek familial cases of Parkinson’s disease, and they
The gene Parkin becomes the first gene associated with juvenile Parkinson’s disease
The gene Parkin provides the instructions for producing a protein that is involved with removing rubbish from within a cell. In 1998, a group of Japanese scientists identified mutations in this gene that resulted in affected individuals being vulnerable to developing a very young onset (juvenile) version of Parkinson’s disease.
The first use of PET scan brain imaging for Parkinson’s disease
Using the injection of a small amount of radioactive material (known as a tracer), the level of dopamine present in an area of the brain called the striatum could be determined in a live human being. Given that amount of dopamine in the striatum decreases over time in Parkinson’s disease, this method of brain scanning represented a useful diagnostic aid and method of potentially tracking the condition.
The launch of Michael J Fox Foundation
In 1991, actor Michael J Fox was diagnosed with young-onset Parkinson’s disease at 29 years of age. Upon disclosing his condition in 1998, he committed himself to the campaign for increased Parkinson’s research. Founded on the 31st October, 2000, the Michael J Fox Foundation has funded more than $700 million in Parkinson’s disease research, representing one of the largest non-governmental sources of funding for Parkinson’s disease.
The Braak Staging of Parkinson’s pathology
In 2003, German neuroanatomist Heiko Braak and colleagues presented a new theory of how Parkinson’s disease spreads based on the postmortem analysis of hundreds of brains from people who had died with Parkinson’s disease. Braak proposed a 6 stage theory, involving the disease spreading from the brain stem (at the top of the spinal cord) up into the brain and finally into the cortex.
The gene DJ1 is linked to early onset PD
DJ1 (also known as PARK7) is a protein that inhibits the aggregation of Parkinson’s disease-associated protein alpha synuclein. In 2003, researchers discovered mutations in the DJ1 gene that made people vulnerable to a early-onset form of Parkinson’s disease.
The first GDNF clinical trial indicates neuroprotection in people with Parkinson’s disease
A small open-label clinical study involving the direct delivery of the chemical Glial cell-derived neurotrophic factor (GDNF) into the brains of people with Parkinson’s disease indicated that neuroprotection. The subjects involved in the study exhibited positive responses to the treatment and postmortem analysis of one subjects brain indicated improvements in the brain.
The genes Pink1 and LRRK2 are associated with early onset PD
Early onset Parkinson’s is defined by age of onset between 20 and 40 years of age, and it accounts for <10% of all patients with Parkinson’s. Genetic studies are finding a causal association for Parkinson’s with five genes: alpha synuclein (SNCA), parkin (PARK2), PTEN-induced putative kinase 1 (PINK1), DJ-1 (PARK7), and Leucine-rich repeat kinase 2 (LRRK2). However it happens, and at whatever age it occurs, there is no doubt that genetics and environment combine together to contribute to the development of Parkinson’s.
The discovery of induced pluripotent stem (IPS) cells
In 2006, Japanese researchers demonstrated that it was possible to take skin cells and genetically reverse engineer them into a more primitive state – similar to that of a stem cell. This amazing achievement involved a fully mature cell being taken back to a more immature state, allowing it to be subsequently differentiated into any type of cell. This research resulted in the discoverer, Shinya Yamanaka being awarded the 2012 Nobel prize for Physiology or Medicine.
2007-2016- Milestones in Parkinson’s Disease Research and Discovery (Part 1e: Historical):
The introduction of the MDS-UPDRS revised rating scale
The Movement Disorder Society (MDS) unified Parkinson’s disease rating scale (UPDRS) was introduced in 2007 to address two limitations of the previous scaling system, namely a lack of consistency among subscales and the low emphasis on the non-motor features. It is now the most commonly used scale in the clinical study of Parkinson’s disease.
The discovery of Lewy bodies in transplanted dopamine cells
Postmortem analysis of the brains of people with Parkinson’s disease who had fetal cell transplantation surgery in the 1980-1990s demonstrated that Lewy bodies are present in the transplanted dopamine cells. This discovery (made by three independent research groups) suggests that Parkinson’s disease can spread from unhealthy cells to healthy cells. This finding indicates a ‘prion-like’ spread of the condition.
SNCA, MAPT and LRRK2 are risk genes for idiopathic Parkinson’s disease
Our understanding of the genetics of Parkinson’s is rapidly expanding. There is recent evidence of multiple genes linked to an increase the risk of idiopathic Parkinson’s. Interestingly, microtubule-associated protein tau (MAPT) is involved in microtubule assembly and stabilization, and it can complex with alpha synuclein (SNCA). Future therapies are focusing on the reduction and clearance of alpha synuclein and inhibition of Lrrk2 kinase activity.
IPS derived dopamine neurons from people with Parkinson’s disease
The ability to generate dopamine cells from skin cells derived from a person with Parkinson’s disease represents not only a tremendous research tool, but also opens the door to more personalized treatments of suffers. Induced pluripotent stem (IPS) cells have opened new doors for researchers and now that we can generate dopamine cells from people with Parkinson’s disease exciting opportunities are suddenly possible.
Neuroprotective effect of exercise in rodent Parkinson’s disease models
Exercise has been shown to be both neuroprotective and neurorestorative in animal models of Parkinson’s. Exercise promotes an anti-inflammatory microenvironment in the mouse/rat brain (this is but one example of the physiological influence of exercise in the brain), which helps to reduce dopaminergic cell death. Taking note of these extensive and convincing model system results, many human studies studying exercise in Parkinson’s are now also finding positive benefits from strenuous and regular exercise to better manage the complications of Parkinson’s.
Transeuro cell transplantation trial begins
In 2010, a European research consortium began a clinical study with the principal objective of developing an efficient and safe treatment methodology fetal cell transplantation in people with Parkinson’s disease. The trial is ongoing and the subjects will be followed up long term to determine if the transplantation can slow or reverse the features of Parkinson’s disease.
Successful preclinical testing of dopamine neurons from embryonic stem cells
Scientists in Sweden and New York have successfully generated dopamine neurons from human embryonic stem cells that can be successfully transplanted into animal models of Parkinson’s disease. Not only do the cells survive, but they also correct the motor deficits that the animals exhibit. Efforts are now being made to begin clinical trials in 2018.
Microbiome of the gut influences Parkinson’s disease
Several research groups have found the Parkinson’s disease-associated protein alpha synuclein in the lining of the gut, suggesting that the intestinal system may be one of the starting points for Parkinson’s disease. In 2016, researchers found that the bacteria in the stomachs of people with Parkinson’s disease is different to normal healthy individuals. In addition, experiments in mice indicated that the bacteria in the gut can influence the healthy of the brain, providing further evidence supporting a role for the gut in the development of Parkinson’s disease.
2016-2017- Milestones in Parkinson’s Disease Research and Discovery (Part 2: Clinical trials either recently completed or in progress)
Safety, Tolerability and Efficacy Assessment of Dynacirc (Isradipine) for PD (STEADY-PD) III trial
Isradipine is a calcium-channel blocker approved for treating high blood pressure; however, Isradipine is not approved for treating Parkinson’s. In animal models, Isradipine has been shown to slow the progression of PD by protecting dopaminergic neurons. This study is enrolling newly diagnosed PD patients not yet in need of symptomatic therapy. Participants will be randomly assigned Isradipine or given a placebo.
Treatment of Parkinson’s Psychosis with Nuplazid
Approximately 50% of the people with Parkinson’s develop psychotic tendencies. Treatment of their psychosis can be relatively difficult. However, a new drug named Nuplazid was recently approved by the FDA specifically designed to treat Parkinson’s psychosis.
Opicapone (COMT Inhibitor) as Adjunct to Levodopa Therapy in Patients With Parkinson Disease and Motor Fluctuations
Catechol-O-methyl transferase (COMT) inhibitors prolong the effect of levodopa by blocking its metabolism. COMT inhibitors are used primarily to help with the problem of the ‘wearing-off’ phenomenon associated with levodopa. Opicapone is a novel, once-daily, potent third-generation COMT inhibitor. It appears to be safer than existing COMT drugs. If approved by the FDA, Opicapone is planned for use in patients with Parkinson’s taking with levodopa who experience wearing-off issues.
Nilotinib (Tasigna® by Novartis) indicates positive results in phase I trial.
Nilotinib is a drug used in the treatment of leukemia. In 2015, it demonstrated beneficial effects in a small phase I clinical trial of Parkinson’s disease. Researchers believe that the drug activates the disposal system of cells, thereby helping to make cells healthier. A phase II trial of this drug to determine how effective it is in Parkinson’s disease is now underway.
ISCO cell transplantation trial begins
International Stem Cell Corporation is currently conducting a phase I clinical cell transplantation trial at a hospital in Melbourne, Australia. The company is transplanting human parthenogenetic stem cells-derived neural stem cells into the brains of people with Parkinson’s disease. The participants will be assessed over 12 months to determine whether the cells are safe for use in humans.
Neuropore’s alpha-synuclein stabilizer (NPT200-11) passes phase I trial
Neuropore Therapies is a biotech company testing a compound (NPT200-11) that inhibits and stablises the activity of the Parkinson’s disease-associated protein alpha synuclein. This alpha-synuclein inhibitor has been shown to be safe and well tolerated in humans in a phase I clinical trial and the company is now developing a phase II trial.
mGluR4 PAM (PXT002331) well tolerated in phase I trial
Prexton Therapeutics recently announced positive phase I clinical trial results for their lead drug, PXT002331, which is the first drug of its kind to be tested in Parkinson’s disease. PXT002331 is a mGluR4 PAM – this is a class of drug that reduces the level of inhibition in the brain. In Parkinson’s disease there is an increase in inhibition in the brain, resulting in difficulties with initiating movements. Phase II clinical trials to determine efficacy are now underway.
Initial results of Bristol GDNF trial indicate no effect
Following remarkable results in a small phase I clinical study, the recent history of the neuroprotective chemical GDNF has been less than stellar. A subsequent phase II trial demonstrated no difference between GDNF and a placebo control, and now a second phase II trial in the UK city of Bristol has reported initial results also indicating no effect. Given the initial excitement that surrounded GDNF, this result has been difficult to digest. Additional drugs that behave in a similar fashion to GDNF are now being tested in the clinic.
Immunotherapies proves safe in phase I trials (AFFiRis & Prothena)
Immunotherapy is a treatment approach which strengthens the body’s own immune system. Several companies (particularly ‘AFFiRis’ in Austria and ‘Prothena’ in the USA) are now conducting clinical trials using treatments that encourage the immune system to target the Parkinson’s disease-associated protein alpha synuclein. Both companies have reported positive phase I results indicating the treatments are well tolerable in humans, and phase II trials are now underway.
Living Cell Technologies Limited continue Phase II trial of NTCELL
A New Zealand company called Living Cell Technologies Limited have been given permission to continue their phase II clincial trial of their product NTCELL, which is a tiny capsule that contains cells which release supportive nutrients when implanted in the brain. The implanted participants will be blindly assessed for 26 weeks, and if the study is successful, the company will “apply for provisional consent to treat paying patients in New Zealand…in 2017”.
MAO-B inhibitors shown to be neuroprotective.
MAO-B inhibitors block/slow the break down of the chemical dopamine. Their use in Parkinson’s disease allows for more dopamine to be present in the brain. Recently, several longitudinal studies have indicated that this class of drugs may also be having a neuroprotective effect.
Inhalable form of L-dopa
Many people with Parkinson’s disease have issues with swallowing. This makes taking their medication in pill form problematic. Luckily, a new inhalable form of L-dopa will shortly become available following recent positive Phase III clinical trial results, which demonstrated a statistically significant improvements in motor function for people with Parkinson’s disease during OFF periods.
Exenatide trial results expected
Exenatide is a drug that is used in the treatment of diabetes. It has also demonstrated beneficial effects in preclinical models of Parkinson’s disease, as well as an open-label clinical study over a 14 month period. Interestingly, in a two year follow-up study of that clinical trial – conducted 12 months after the patients stopped receiving Exenatide – the researchers found that patients previously exposed to Exenatide demonstrated significant improvements compared to how they were at the start of the study. There is currently a placebo-controlled, double blind phase II clinical trial being conducted and the results should be reported before the end of 2017.
A personal reflection
As I suggested at the start of this post, this endeavour was entirely Frank’s idea – full credit belongs with him. I was more than happy to help him out with it though as I thought it was a very worthy project. During this 200 year anniversary, I believe it is very important to acknowledge just how far we have come in our understanding of Parkinson’s disease since James first put pen to paper and described the six cases he had seen in London.
And Frank’s idea perfectly captures this.
The banner for today’s post was sourced from Greg Dunn (we are big fans!)
Our policy at the SoPD is not to advertise or endorse commercial products or services. This is to avoid any ethical or conflict of interest situations.
Every now and then, however, we see something that we believe will be of interest and value to the Parkinson’s community…aaand we bend our policy rule book.
Today the Journal of Parkinson’s disease released a “200 years of Parkinson’s disease” OPEN ACCESS special issue of their journal which highlights some of the major discoveries in the field of Parkinson’s disease research.
Critically, the articles provide insights into how the discoveries were made, and they are written by some of the biggest names in the Parkinson’s research community (many of whom were actually there when the discoveries were made).
The issue has articles dealing with topics including:
Click here to see all of the articles in this special issue.
We fully recommend readers take advantage of this OPEN ACCESS issue and learn about how some of these great discoveries were made.
Full disclosure: The Journal of Parkinson’s disease is a product of IOS Press. The SoPD has not been approached by or made any offers to IOS Press or anyone at the Journal of Parkinson’s disease. We merely thought that the material in this particular OPEN ACCESS issue would be of interest to our readers.
The banner for today’s post was sourced from the Journal of Parkinson’s disease
On the 8th September 2015, we kicked this blog off with the goals of:
- Trying to answer any questions you may have about Parkinson’s disease.
- Report each week on interesting/exciting research in the world of Parkinson’s disease.
- Interview Parkinson’s disease researchers, providing a face to the people doing the work.
- Help you to understand this disease better.
On the first goal, we have fielded many questions and hope that we have provided satisfactory answers (thus far, no complaints). On the second, we are pleased to have published 63 posts over the past year – more than once per week (rather miraculous considering the requirements of work and family). As for interviewing researchers, we have held back on this, but will be looking to initiate something in this next 12 months – it is a question of format rather than availability of interviewees. We are thinking about posting some videos and this may be a better format for readers to meet the researchers behind the science.
On the final goal, well… only you the reader can judge how we are doing in that regard. We hope that we are providing useful information.
Looking forward to another year of Parkinson’s Science!
The banner for today’s post was sourced from PlusQuotes