Monthly Research Review – April 2018

At the end of each month the SoPD writes a post which provides an overview of some of the major pieces of Parkinson’s-related research that were made available during April 2018.

The post is divided into five parts based on the type of research (Basic biology, disease mechanism, clinical research, other news, and a new feature: Review articles/videos). 

So, what happened during April 2018?

In world news:

  • April 4–15th – The 2018 Commonwealth Games were held in Gold Coast, Queensland, Australia (New Zealand came 5th in the medals tally… not bragging, just saying).

Source: Vimeo

  • April 27th – Kim Jong-un crosses into South Korea to meet with President Moon Jae-in, becoming the first North Korean leader to cross the Demilitarised Zone since its creation in 1953. In initial small steps towards reconciliation, South Korea said it would remove loudspeakers that blare propaganda across the border, while North Korea said it would shift its clocks to align with its southern neighbour.

BFFs? Source: QZ

Source: Plus

  • And finally the city of Trier in Germany is already struggling to keep up with demand for ‘0-euro’ notes, bearing the face of its most famous son and communism’s creator Karl Marx. Sold for 3 euros each, the notes are part of celebrations for his 200th birthday (5th May 1818).

You get what you pay for. Source: DDR

In the world of Parkinson’s research, a great deal of new research and news was reported:

In April 2018, there were 655 research articles added to the Pubmed website with the tag word “Parkinson’s” attached (2924 for all of 2018 so far). In addition, there was a wave to news reports regarding various other bits of Parkinson’s research activity (clinical trials, etc).

April also represented Parkinson’s Awareness month, with many activities going on world wide to raise awareness about the condition. One of my favourites was the Parkinsons Awareness Month Haiku Competition being run by World Parkinson’s Congress. A haiku is a 17 syllable poem (usually in a 5x7x5 format).

This was my best effort:

Title: ‘G2019S’
Lurking silently
A hyperactive protein
needs inhibition

My second best effort:

Think I’m going mad
Now seeing world through haiku
Thank you WPC

The top 5 pieces of Parkinson’s news

1. Heart failure treatment for Parkinson’s?

Researchers in France report that NKCC1 chloride importer antagonist, Bumetanide, provides a novel therapeutic strategy for Parkinson’s based on a restoration of low chloride levels which corrects GABAergic inhibition and improves motor ability in a mouse model of Parkinson’s ( to read the research report and click here to read a SoPD post on the topic). Bumetanide is a clinically available drug used to treat heart failure. Some side effects (exacerbates diabetes & gout). The researchers are attempting to start a phase II clinical trial for Bumetanide in Parkinson’s following a small pilot study:

2. Inflammatory bowel disease, Parkinson’s and anti-TNF therapy

Researchers report that individuals with inflammatory bowel disease (IBD) have 28% higher risk of developing Parkinson’s. They also found a lower rate of PD among people with IBD who were exposed to anti-TNF therapy vs those not ( to read more about the research and Click here to read a SoPD post on the topic).

3. Novel class of enzyme – Novel therapeutic angle for Parkinson’s

Scottish researchers has discovered a novel class of E3 ligase (one of the enzymes involved in ubiquitination). Inactivation of this particular enzyme could have therapeutic potential for neurodegenerative conditions like Parkinson’s ( to read the abstract of this research). Ubiquitination is the process of attaching a small protein, ubiquitin, to target proteins which helps alter function and outcome of the protein. E3 ligases are enzymes involved in this process. MYCBP2, however, works differently to the other classes of E3 ligase. Importantly MYCBP2 activity has been shown to drive the degeneration of neurons hence the potential therapeutic angle for Parkinson’s. Great story behind the discovery – ‘dream come true moment’ for the PhD student (Click here to read the press release).

Source: Mycancergenome

4. I’ll have the fish please

Swedish researchers found that a fish-derived protein called β-parvalbumin readily inhibits the formation of the aggregated form of Parkinson’s-associated alpha synuclein. The researchers naturally ask if “fish intake may provide health benefits” for people with Parkinson’s ( to read the full report).

5. Diabetes and Parkinson’s

New research finds that diabetes mellitus may predispose individuals toward Parkinson’s-like pathology, & when present in people with PD, it is associated with faster motor progression ( to read the abstract to this research and click here to read an SoPD post on this topic).

Basic biology news

  • Researchers have been exploring the role of post‐translational modifications in regulating Parkinson’s-associated alpha synuclein protein interactions using nanobodies ( to read more about this).
  • The cholesterol metabolite 27-hydroxycholesterol (27-OHC) has been found to act as a factor that can increase levels of Parkinson’s-assocaited alpha synuclein and the inhibition of the proteasomal function (the waste disposal process of the cell;  to read about this research).
  • A protein called Triggering receptor expressed on myeloid cells-2 (TREM2) has been found to plays a crucial role in altering microglial cells – immune cells in the brain – from an inflammatory M1 to an immunosuppressive M2 state in models of Parkinson’s ( to read that research report).
  • Interesting new tool (DNP-Enhanced MAS NMR) allows for quantitative information regarding the structural changes of the different states of Parkinson’s-associated protein alpha synuclein ( to read more about this).

  • The dynamics of Parkinson’s-associated protein PARKIN have been revealed by digital snapshot proteomics. Analysis of PARKIN-dependent mitochondrial ubiquitylation in induced neurons & model systems ( to read more about this).
  • Interesting new manuscript on BioRxiv looking at the small heat-shock protein αB-crystallin which is associated with both Alzheimer’s and Parkinson’s. αB-crystallin reduces toxicity of aggregating amyloid proteins ( to read the manuscript).
  • Chemical reprogramming of astrocytes (the supportive helper cells) into functional neurons inside the brains of mice. New BioRxiv manuscript demonstrates in vivo chemical reprogramming in the adult brain – a novel therapeutic approach for Parkinson’s? ( to read the manuscript).
  • Small Parkinson’s-associated alpha synuclein protein oligomers are difficult to isolate for analysis. Researchers have gained better insight into the properties of these small oligomers by linking them head-to-tail (in tandem) & comparing the behaviour. Clever trick ( to read the research report).
  • Human islet amyloid polypeptide (or amylin) has the tendency to aggregate in diabetes. High levels of amylin have been found to cause similar changes in mitochondrial dynamics to that caused by Parkinson’s-associated alpha synuclein. Coincidence? ( to read the research report).

  • Lysosomal Therapeutics researchers provide new mechanistic insights into Glucocerebrosidase (GBA) enzyme activity, which facilitates the rational design of novel GCase modulators for Gaucher disease & Parkinson’s.The researchers developed a potent quinazoline modulator, JZ-4109, which stabilises WT and N370S mutant GCase & increases GCase abundance in patient-derived cells. They also developed a modification strategy using a lysine targeted inactivator (JZ-5029) for in vitro studies ( to read more about this).
  • Recent studies have found an age-dependent reduction in Parkinson’s-associated Glucocerebrosidase (GBA) GCase enzyme activity & elevation of some glycosphingolipid (GSL). New research finds GSL levels are increased with age in mice, while GCase is reduced. Lipid alterations in Parkinson’s? ( to read the research report).
  • Distinct copies (or isoforms) of RNA can come 1 gene. They encourage diversity, but they are difficult to characterise in sequencing studies because of shared subsequences. BIISQ is a new model for identifying different RNA isoforms. A useful tool for Parkinson’s research ( to read the research report).

Source: Youtube

Disease mechanism

  • Exosomes are cell-derived nano (50–150 nm) bags, which mediate communication between cells. Researchers describe EXOsomal transfer into cells (EXOtic) devices for use against models of Parkinson’s ( to read this report).
  • Parkinson’s-associated aggregated alpha synuclein protein isolates synaptic proteins leading to neurotoxicity. A new blocking peptide (P5) derived from VAMP2 partially blocks this process & reduces neurotoxicity ( to read the full report).
  • Glial cell-derived neurotrophic factor (GDNF)-producing macrophages (blood cells, introduced via bone marrow cell transplantation) reduce the loss of dopamine neurons and improve Parkinson’s motor symptoms in a genetic mouse model of PD (MitoPark mice;  to read more about this).
  • New manuscript on the BioRxiv website suggests model by which the toxic form of Parkinson’s-associated alpha synuclein protein (oligomers) occurs via cell membrane-mediated aggregation ( to read that manuscript).
  • SNARE proteins mediate membrane fusion events within cells. New research finds that calcium enhances SNARE-mediated membrane fusion that is inhibited by Parkinson’s-associated protein alpha synuclein ( to read the abstract of this research).

  • Nurr1 is a protein that is critical for the survival of dopamine neurons. New research suggests that small ligand C-DIM12 is an activator of Nurr1 that suppresses glial activation & protects dopamine neurons in a model of Parkinson’s ( to read more about this).
  • New study reports that mice with no Cx3cr1 protein have an exaggerated response to neuroinflammation induced by mutant form of Parkinson’s-associated alpha synuclein, resulting in more dopamine cell loss ( to learn more about this research).
  • Sulfated polysaccharides (a kind of carbohydrate isolated from algae) have been found to effectively inhibit the fibrillation of Parkinson’s-associated protein Alpha Synuclein. Therapeutic implications? ( to read the research report).
  • New research reports the existence of a novel soluble α‐helical conformer of Parkinson’s-associated protein Alpha Synuclein, obtained through transient interaction with lipid interfaces. Dynamic oligomerization may be a mechanism underlying its stability ( to find out more about this).
  • New study supports for the involvement of the NFE2L2 and PPARGC1α genes in Parkinson’s susceptibility & progression, through pathways involving maneb & paraquat pesticide exposure ( to read more).

Pesticide exposure. Source: FT

  • A novel mechanism by which extracellular levels of Parkinson’s-associated alpha synuclein protein could be influencing PD pathogenesis (driving sphingosine 1-phosphate receptor subtype 1 out of lipid rafts & leading to impaired G protein signaling –  to read about this research).
  • By increasing levels of DJ-1 protein in astrocytes (the helper cells in the brain), researchers rescue rodent model of Parkinson’s, by reducing inflammation & decreasing alpha synuclein accumulation in dopamine neurons ( to read more about this).
  • Degradation of Parkinson’s-associated alpha synuclein protein by increasing levels of dendritic cell factor 1 (DCF1) delays neurodegeneration and extends lifespan in flies (drosophila). DCF1 could degrade alpha synuclein both in vivo & in vitro ( to read more).
  • Tauroursodeoxycholic acid (TUDCA) is the taurine conjugate form of ursodeoxycholic acid (UDCA) which is being tested for Parkinson’s. New research suggests TUDCA is also neuroprotective in models of PD (Paris inhibitor; DJ-1 activator –  to read the abstract of this research and click here to read a SoPD post on this topic).

  • A meta-analysis of publicly available microarray data has been published which identifies biological regulatory networks in Parkinson’s blood & brain samples. 53 differentially expressed genes in PD patients vs controls (including some PD-specific miRNAs –  to learn more about this research).
  • New manuscript on the BioRxiv website investigates neuroprotective effect of beta synuclein in a model of Parkinson’s. Beta synuclein is the sister protein to alpha synuclein. Beta syn had no rescue effect. In fact, it started to aggregate as well! ( to read the manuscript).
  • 2-Pentadecyl-2-Oxazoline, a oxazoline derivative of the fatty acid amide signalling molecule palmitoylethanolamide (PEA) has been found to activate of antioxidant nuclear factor E2-related factor 2 (NRF2) in models of Parkinson’s ( to read more about this).
  • Parkinson’s-associated PARKIN deficiency exacerbates NLRP3 inflammasome activation by specific inducers in microglia & bone marrow‐derived macrophages ( to read more about this).
  • p27Kip1 regulates Parkinson’s-associated alpha synuclein expression. Knock-down of the member of the same family p21Cip1(p21) also led to increased α-synuclein levels, indicating that p27 & p21 collaborate in the repression of alpha synuclein transcription ( to read the research report).
  • Green tea ingredient EGCG (EpiGalloCatechin-3-Gallate) found to protect & prevent oxidative stress & neurodegeneration in a genetic fly model of Parkinson’s ( to read more about this research)

Green tea for EGCG

  • Researchers have demonstrated that the sustained level of a protein called astrocyte elevated gene-1 (AEG-1) is an important anti-apoptotic mechanism for dopamine neurons in models of Parkinson’s, may potentiate the therapeutic effects of other treatments ( to read this research report).
  • Deficiency in a protein called Seipin in mice causes loss of dopamine neurons via aggregation & phosphorylation of Parkinson’s-associated alpha synuclein & inflammation ( to read this research report).
  • 256750 molecules were virtually screened for their binding activities as MAO-B inhibitors (a common Parkinson’s medication). The top hit displayed higher selectivity towards MAO-B than the positive control (Selegiline – a commonly used MAO-B inhibitor –  to read more about this research).
  • Gintonin, a neuroprotective component of ginseng, has been found to reduce dopamine cell loss & accumulation of alpha synuclein (via the Nrf2 pathway) in model of Parkinson’s ( to learn more about this).

Ginseng. Source: Wholefoodsmagazine

  • In a new manuscript on BioRxiv, researchers used high-resolution metabolomics to identify compounds & pathways that differ between people with Parkinson’s & control subjects, including harmalol & the glycosphingolipid pathway ( to read the manuscript).
  • Parkinson’s-associated alpha synuclein oligomers cause oxidative stress leading to changes in PARKIN protein, resulting in the degradation of the protein. This decrease in PARKIN levels = increased cell death. Increasing PARKIN levels helps the situation ( to read more about this).
  • Researchers report that increasing levels of alpha synuclein in the subthalamic nucleus can cause Parkinson’s-like burst firing activity. PFE-360, a brain-penetrating LRRK2 inhibitor, reverses the firing effect, but is not neuroprotective ( to learn more about this).
  • Parkinson’s-related changes (‘nitration’) to microtubules inside the branches of neurons blocks mitochondrial transport in a human pluripotent stem cell collected from people with SNCA-A53T-associated PD. Effects were rescued by NOS inhibitor ( to read more about this).
  • Researchers from the Netherlands demonstrate that a drug KH176 that biotech firm Khondrion is developing for Parkinson’s can effectively reduce oxidative stress levels in primary cells derived from people with mitochondrial conditions ( to read the research report).


  • Researchers use Rabies Virus Glycoprotein 29 attached to a nanoparticle filled with Deferoxamine (an iron chelator) to reverse the functional deficits associated with a mouse model of Parkinson’s ( to learn more about this).
  • Delta opioid receptor agonist UFP-512 reverses cell based model of Parkinson’s. This DOR-mediated protection appears to require PD-associated protein PINK1 ( to read more about this).
  • No significant differences found in levels of neurogranin in the cerebrospinal fluid between the different types of Parkinson’s (corticobasal syndrome, progressive supranuclear palsy, & dementia with Lewy bodies). Useful biomarker for Alzheimer’s? ( to read the abstract of this research).

Clinical research

  • Application of the Movement Disorder Society prodromal criteria in first‐degree relatives of Ashkenazi Jewish people with G2019S‐LRRK2-associated Parkinson’s identifies 17 probable cases of PD in this high risk cohort – early diagnosis tool? ( to learn more about this research).
  • Aussie researchers show that many people in a representative cohort of Parkinsons benefit from objective assessment & treatment of their PD features against a target ( to read the report).
  • Chinese researchers report that a genetic variant (rs823114) in the NUCKS1 gene decreases risk of developing Parkinson’s & shows a male genetic distribution bias in the Han Chinese population ( to read more about this).
  • 154 people with PD were assessed. 90 of them were found to have abnormal insulin resistance. Interesting study providing further support for the high prevalence of undiagnosed Insulin resistance in non-diabetic people with Parkinson’s ( to read more about this).
  • Interesting report on the long-term satisfaction & patient-centered outcomes of bilateral subthalamic nucleus deep brain stimulation in Parkinsons ( to find out more about this).
  • New meta-analysis study determines a personality profile associated with Parkinson’s, which may occur in the pre-motor stages – apparently folks at risk at high in neuroticism & harm avoidance; and low in openness, extraversion & novelty seeking ( to learn more about this).

Personality. Source: FT

  • Urate is a salt derived from uric acid. High urate levels have been associated with lower risk of Parkinson’s. New study suggests this association is consistent among men & less clear among women. A protective effect of urate among women after menopause ( to read more about this).
  • 3206 people with Parkinson’s involved in a multi-centre evaluation of the relationship between the MDS-UPDRS and Quality of Life (QoL) assessments. Highlights the importance of non-motor features on QoL ( to find out more about this research).
  • New study assesses the diagnostic accuracy of the trophy of the “hummingbird sign” & the “morning glory flower sign” in brain imaging. Finds it highly specific for progressive supranuclear palsy (PSP), a form of Parkinsonism – similar to Parkinson’s ( to learn more).
  • Lower-limb peripheral neuropathy is associated with more falls and gait issues in Parkinson’s. Fall prevention strategies for PD should consider peripheral neuropathy. Evaluation of lower-limb peripheral neuropathy is important ( to learn more).
  • Using smartphones & machine learning to quantify Parkinson’s. New study measured 5 tasks (voice, finger tapping, gait, balance, & reaction time) & found measures provided objective, real-world assessments 4 enhancing clinical care & evaluation ( to read more about this research).

  • Researchers recruited 304 Dutch people with Parkinson’s from the Parkinson@Home study and used wearable sensors to quantity gait. They found that the severity of motor fluctuations did not correlate with time spent walking ( to learn more about this study).
  • Italian researchers found that autonomic dysfunctions & depressive symptoms represent the leading determinant of non-motor symptom clusters in Parkinson’s. They propose a “neurotransmitter-based” model ( to read more about this research).
  • Researchers compared motor & non-motor features of Parkinson’s in LRRK2-G2019S genetic mutation carriers vs non-carriers. Found no significant difference btwn LRRK2+ PD subjects & LRRK2- PD controls in UPDRS, MoCA, or other motor/non-motor endpoints ( to read about this study).
  • New bioinformatics research (big dataset of  82,337 cases & controls) reveal common pathways between different neurodegenerative conditions, including Parkinson’s. Also highlights the strong physical interactions between CXCR4 & four microglia related genes ( to read more about this work).
  • The genetic overlap between ALS, frontotemporal dementia (FTD), Parkinson’s, Alzheimer’s & other neurodegenerative conditions (124 876 cases & controls) finds common genetic pathways between ALS & FTD. MAPT & BNIP1 influence the pathogenesis of ALS ( to learn more).
  • Very interesting review of the “genotype‐phenotype” relationships for the Parkinson’s. University of Luebeck researchers outline what is known about the PD features associated with genetic variants in three PD-associated genes: PARKIN, PINK1, & DJ1 ( to read more about this research).

  • “Known protective factors for Parkinson’s tend to have additive or superadditive effects, so that PD risk is very low in individuals with multiple protective risk factors” – the conclusion of a new prospective examination of lifestyle/family factors in PD. From 2,652,243 person-years of follow-up: “Our results show that the risk score was associated with decreased risk of Parkinson’s, and that the combination of family history & known lifestyle factors can explain 80% of cases of PD in men and 63% in women” ( to read the abstract about this research).
  • researchers report the onset of a new functional movement disorder in 4 cases of Parkinson’s after successful deep brain stimulation. Resolution of functional symptoms occurred within 3 months in all cases ( to learn more).
  • Interesting analysis of non-motor outcomes after subthalamic deep brain stimulation in Parkinson’s – results suggest it all depends on the location of active contacts ( to read more about this).
  • New study calls for interventions addressing caregiver burden in Parkinson’s with deep brain stimulation that target those with greater symptomatology at baseline & may be usefully to prioritise psychiatric symptoms reported by the caregiver ( to read this article).
  • Further evidence of an association between REM sleep behaviour disorder and Parkinson’s ( to read the abstract of this report).

REM sleep behaviour disorder

  • After analysing lifestyle factors from 1997 to 2010 in a cohort of 41,638 Swedish men & women, researchers find no association between prolonged sitting time per day or obesity & risk of developing Parkinson’s ( to read the abstract of this report)
  • New study provides further support for recommending physical activity to diminish risk of Parkinson’s. High physical fitness, current smoking & younger age were associated with a lower incidence ( to read more about this).
  • New research suggests that the semantic fluency deficit in Parkinson’s has a strategic component. PD subjects sequences were less semantically organised than controls, but this effect is only in the smaller category (fruits) ( to read more).
  • 27 people with Parkinson’s. Divided into three equal groups: (a) Nintendo Wii™, (b) Xbox Kinect™, and (c) control group. 10 sessions playing four physical games. Only those engaged with Nintendo Wii™ exhibited beneficial results (motor, anxiety, memory –  to read more about this research).

  • Using the Veterans Health Administration databases (from October 2002 to September 2014), researchers have found mild traumatic brain injury is associated with 56% increased risk of Parkinson’s ( to read the abstract of this report).
  • New BioRxiv manuscript suggests that people with early-stage medicated Parkinson’s show lower task-related functional connectivity but not activity of brain regions that are important for response inhibition. Medication upheld task-related activity? ( to read the manuscript).
  • Amyloid deposits are common in dementia with Lewy bodies (DLB; similar to Parkinson’s), but its significance is unclear how they relate to the condition. New brain imaging study finds that amyloid deposits are not associated with differences in clinical or neuropsych profiles in DLB ( to read more about this).
  • A 4 year study found that people with Parkinson’s exhibit decreased regularity of trunk dynamics when standing compared to healthy controls ( to learn more about this).
  • Interesting new manuscript on BioRxiv analysed bacteriophage composition of the fecal samples from people with drug-naive Parkinson’s (vs healthy controls) – they reveal significant alterations (

Bacteriophage attacking a bacteria. Source: Sci-news

  • 17 new genetic risk factors for Parkinson’s were recently identified in caucasian population. Now Chinese researchers report no association between the 5 most common of these new genetic variants in Chinese cohorts of PD or multiple system atrophy ( to read the research report).
  • A longitudinal 36-month study finds that degeneration (lower grey matter volume) of a region of the brain called the nucleus basalis of Meynert precedes & predicts the onset of cognitive impairment in Parkinson’s ( to read the abstract of this research report).
  • Using high definition EEG, researchers found a differing topography of cerebellar activity in Parkinson’s, essential tremor & mimicked tremor (in health controls –  to read the abstract of this research report).
  • ICICLE-PD researchers look at whether white matter microstructural changes can be used as a predictor of worsening of motor features or cognitive decline in Parkinson’s. Diffusion tensor imaging is potentially a useful tool for stratification of PD ( to read the abstract of this research report).
  • New BioRxiv manuscript describes neuropathological & cognitive performance in 40 centenarians. Alzheimer’s-associated pathology (Aβ & Tau) were abundant, whereas Parkinson’s-associated pathology (eg Lewy bodies) = scarce ( to read the manuscript). Compare the Alzheimer’s-associated Beta amyloid graph in panel D with Parkinson’s-associated Lewy body graph in panel J. The one case with significant Lewy body pathology (the out of 26 analysed) was actually diagnosed with PD many years before the study started.
  • Subtyping Parkinson’s – 192 people with de novo Parkinson’s were divided into the tremor-dominant/mixed/akinetic-rigid (TD/mixed/AR) or tremor-dominant/mixed/postural instability and gait disturbance (TD/mixed/PIGD) subtypes. PIGD subtype showed more severe non-motor symptoms ( to read the abstract of this research report).

Clinical trial news

  • A demonstration of how the eradication of small intestinal bacterial overgrowth (SIBO) with rifaximin, a non-absorbable antibiotic, improved motor fluctuations in people with Parkinson’s in a small (n = 14) unblinded, non-randomized clinical study ( to read more about this).
  • A randomised, double-blind study on 20 people with Parkinson’s and subthalamic deep brain stimulation finds a wide range of frequencies are efficacious in improving upper-limb motor function ( to learn more).

Deep brain stimulation

  • A Phase I clinical study in healthy volunteers assessed the safety, tolerability, pharmacokinetics & bioavailability of ND0701, a novel formulation of apomorphine for subcutaneous infusion for Parkinson’s. Direct comparison made with APO-go® ( to read the abstract of this study).
  • An 8-week low-intensity progressive cycling training improves motor functions in people with early-stage Parkinson’s (13 people took part in 16 serial cycling sessions over a 2-month period; not blinded –  to read the research report).
  • 12 month clinical study of Istradefylline (a adenosine A2A receptor antagonist) was found to improve not only Parkinson’s motor symptoms, but also lower urinary tract symptoms (significantly at 3 months’ administration) ( to read more about this).
  • Biotech firm Theranexus announces that they have received European approval for a Phase II clinical trial of their combination drug THN102 (Modafinil/Flecainide) for excessive daytime sleepiness associated with Parkinson’s ( to read the press release).

  • New findings from the multicenter, prospective INTREPID study, presented at the annual meeting of the American Academy of Neurology. 292 people with Parkinson’s across 23 US sites, evaluating independently controllable current on 8 electrodes for deep brain stimulation ( to read the press release).
  • A 12 months extension study looking at the use of Opicapone, a COMT inhibitor, finds that it is well tolerated & reduces “OFF” time in 495 people with Parkinson’s. Switching from entacapone to opicapone led to enhanced efficacy ( to read more about this research).
  • Intec Pharma presented Phase 1 pharmacokinetics and safety data regarding Accordion Pill Carbidopa/Levodopa at American Academy of Neurology Annual Meeting ( to read the press release).

Other news

  • A new study provides the first comprehensive estimates of health care costs in people with Parkinson’s based on routinely collected data. Health care costs attributable to PD increase in the year following diagnosis & are higher for people with complications ( to learn more about this).
  • The Michael J. Fox Foundation has launched “Parkinson’s Clinical Trial Companion” – an educational suite designed to support progress in Parkinson’s research by increasing patient participation in clinical studies – a worthy idea! ( to read more about this).

  • Interesting write up from the Advances in Alzheimer’s and Parkinson’s Therapies Focus meeting (AAT-AD/PD) meeting in Turin (Italy) regarding efforts to target tau in Alzheimer’s and Parkinson’s ( to read that article).
  • Global Kinetics Corporation has been awarded grants from Michael J Fox Foundation, Shake It Up Australia & Parkinson’s Victoria to advance management & outcomes in Parkinson’s ( to read the press release).
  • The Parkinson’s UK and University of Sheffield virtual biotech firm Keapstone Therapeutics has a new website – fascinating biotech venture focused on small molecule activators of the Nrf2-ARE pathway 4 neuroprotection in Parkinson’s & Amyotrophic Lateral Sclerosis (ALS) – 

I am adding a new topic to the monthly research review, for those seeking general information on topics of Parkinson’s research:

Review articles/videos

  • The asymmetry of dopaminergic neurodegeneration & the subsequent lateralisation of motor symptoms are distinctive features of many cases of Parkinson’s. This interesting review thoroughly explores this topic ( to read more).
  • A fantastic, easy-to-read write up by Kevin McFarthing explaining the biology of what goes wrong in cells in Parkinsons ( to read the write up).
  • It is fair to say that the god father of neurology Jean-Martin Charcot did as much for Parkinson’s as James himself did. Now a fascinating write up by Dr. Olivier Walusinski about Charcot & his teachings has been published. Brilliant historical insights ( to read this review).

Jean-Martin Charcot

  • Interesting talk last week from Prof Roger Barker at the Cure Parkinson’s Trust research update meeting – Spring 2018:
  • Also an interesting talk from Prof Huw Morris at the the Cure Parkinson’s Trust research update meeting – Spring 2018:
  • An interesting mini review about the function of Parkinson’s-associated protein PARKIN in the context of PD ( to read the review)

  • Iranian & UK researchers provide a very thorough review covering the genetic components of Parkinson’s – from Mendelian forms to genetic susceptibility: New molecular insights into the neurodegenerative process ( to read this review).
  • An excellent, open access review of the development of targeted therapies for Parkinson’s – discussing the move from genetics to the clinic with novel therapies that have been designed around the biology of PD
    (Click here to read the review).

* * * * * * * * * * * * * * *

And there it is, just some of the highlights from April 2018 – another very busy month of Parkinson’s research. Hopefully there will be bits and pieces of interest for everyone in the list. Much of the material used here was collected from the Science of Parkinson’s Twitter feed (and there is a lot more posted there each day).

Any thoughts/feedback would be greatly appreciated (either in the comments below, or contact me directly).

And now: on to May! (can you believe IT’S MAY!!! Already?!?)

EDITOR’S NOTE: The information provided by the SoPD website is for information and educational purposes only. Under no circumstances should it ever be considered medical or actionable advice. It is provided by research scientists, not medical practitioners. Any actions taken – based on what has been read on the website – are the sole responsibility of the reader. Any actions being contemplated by readers should firstly be discussed with a qualified healthcare professional who is aware of your medical history. While some of the information discussed in this post may cause concern, please speak with your medical physician before attempting any change in an existing treatment regime.

In addition, many of the companies mentioned in this post are publicly traded companies. That said, the material presented on this page should under no circumstances be considered financial advice. Any actions taken by the reader based on reading this material is the sole responsibility of the reader. None of the companies have requested that this material be produced, nor has the author had any contact with any of the companies or associated parties. This post has been produced for educational purposes only.

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