Monthly Research Review – September 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 September 2018.

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

So, what happened during September 2018?

In world news:

September 2nd – A fire destroyed the National Museum of Brazil in Rio de Janeiro –  a “catastrophic loss of artifacts”.

Source: HuffPost

September 14th – Hurricane Florence made landfall in Wrightsville Beach (North Carolina), caused extensive damage and flooding throughout in the Carolinas.

Source: WPLG

September 17th – In an effort to study the hidden physical properties of electrons, Japanese researchers built the ‘most powerful magnet on Earth’ – a 1200 Tesla, 3.2 megajoules beast. The experiment was supposed to go off with a bang, but the ‘bang’ was slightly more than expected: it blew the door off the protective chamber holding the experiment!

September 21st – after a three year journey, the first rover of the Japanese Hayabusa2 spacecraft touched down on the surface of the asteroid Ryugu. A truly remarkable achievement.

Source: NYTimes (some amazing images on this link)

September 24th – Two reports were published – one in the journal Nature Medicine and another in the journal New England Journal of Medicine – describing the case of 29-year-old Jered Chinnock (who 5 years ago could not feel or move his body from the chest down) recovering the ability of assisted walking following spinal cord stimulation and intensive physical therapy.

September 28th – A magnitude 7.5 earthquake hit the island of Sulawesi (Indonesia), causing a tsunami and terrible destruction and loss of life.

Source: Australian


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

In September 2018, there were 841 research articles added to the Pubmed website with the tag word “Parkinson’s” attached (5978 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).

The top 5 pieces of Parkinson’s news

1. 746,000!!!

A large consortium of academic and biotech researchers conducted a HUGE screening experiment to identify compounds that markedly inhibit the clustering (or aggregation) of Parkinson’s-related alpha synuclein. They screened 746,000 compounds – yes, 3/4 of a million compounds and identified 58 compounds that reduce aggregation as well as 100 compounds that increase it. Most effective aggregation inhibitors were derivatives of (4-hydroxynaphthalen-1-yl)sulfonamide. But of particular interest to us was the positive control compounds they used: Epigallocatechin Gallate (or EGCG) and baicalein ( to read more about this, and click here to read an SoPD post on this study).

2. ADHD and Parkinson’s

New research was published suggesting that people with Attention Deficit Hyperactivity Disorder (or ADHD) may be twice as likely as members of the general public to go on to develop Parkinson’s-like conditions. And this risk increases to 4x normal rates in individuals with ADHD who were treated with stimulant medication. The researchers found that of the 31,769 people with ADHD, only 56 went on to develop Parkinson’s (0.18% of the total group), compared to 96 (0.06%) of the control group (non-ADHD; 158,790 individuals). And of the 4,960 records of people with ADHD who were prescribed stimulant medications in this study, only 19 were subsequently diagnosed with PD ( to read more about this and click here to read a SoPD post on this topic).


3. Smart (phone) diagnostic aid

Researchers found that consumer grade smartphones can be used to accurately separate not only people with idiopathic REM sleep behavior disorder (iRBD – which is thought to be a precursor to PD) from controls, but also iRBD from Parkinson’s ( to read more about this).


4. Shifting to the nucleus makes a big difference

Movement of Parkinson’s-associated alpha synuclein to the nucleus is modulated by a process called phosphorylation (a modification of a particular location on the protein). Researchers have found that the toxicity of alpha synuclein in models of Parkinson’s may be regulated by shift to the nucleus and this nuclear presence of alpha synuclein protein ( to read more about this).


5. Salbutamol

A recent study observed a 2x greater risk of Parkinson’s in users of the blood pressure drug propranolol, and a lower risk of PD for the asthma medication salbutamol. Both drugs work via interactions with a molecule called β2-adrenoreceptor. BUT a new case-control study of US Medicare beneficiaries has FAILED to replicate the result ( to read more about this and click here to read a SoPD post on the topic).


Basic biology news

  • STAT3 & Sox9 may be the independent targets of Parkinson’s-associated protein DJ-1. Inhibition of STAT3 attenuates astrogliosis & reduces BDNF/GDNF levels in brain slices, similar to DJ-1 knockout ( to read more about this).
  • A rapid, reversible, & tunable method of stabilising proteins (called destabilizing domain degron technology) has been applied to Parkinson’s-related GNDF with interesting results ( to read more about this).
  • New manuscript on biorxiv suggests that Parkinson’s-associated alpha synuclein binds to extracellular complex N-linked glycans. Cellular internalization of both normal & toxic forms of α syn is reduced dramatically upon removal of N-linked glycans ( to read more about this).
  • The toxic twosome? Researchers present findings that Parkinson’s-associated alpha synuclein induce a distinct toxic Tau oligomeric protein strain that avoids fibril formation, & accelerated an Alzheimer’s mouse model ( to read more about this).
  • Potent PDZ-Domain PICK1 inhibitors have been identified that modulate Alzheimer’s-related amyloid beta-mediated synaptic dysfunction. Given that PARKIN regulates PICK, perhaps these inhibitors could be interesting for Parkinson’s? Just saying ( to read more about this & click here for the PARKIN-PICK1 research).
  • Researchers got up close & personal (atomically close) with Parkinson’s-associated alpha synuclein protein; identifying new areas that could be targeted with new therapies ( to read more about this).
  • An analysis of the effect of exposing different species (monomeric, oligomeric, & fibrillar) of Parkinson’s-associated alpha synuclein protein to astrocytes (the supportive cells in the brain) finds all of them increased activation of the cells, but only oligomers induced mitochondrial dysfunction ( to read more about this).
  • Low-dose aspirin increases dopamine levels in both cell cultures and mice (normal & PD model), via by up-regulation of the tyrosine hydroxylase enzyme. Implications for Parkinson’s? ( to read more about this, and click here to read a SoPD post on this topic).


  • A new genetic variation in the SYNJ1 gene has been discovered in a Tunisian family, which is associated with juvenile onset Parkinson’s & epilepsy ( to read more about this).
  • Parkinsons-linked PARKIN mutations impair glutamatergic signaling in hippocampal neurons, by impeding NMDA and AMPA receptor trafficking ( to read more about this).
  • Parkinson’s-associated alpha synuclein disrupts the function of β-arrestin2 and increases inflammation in the pathogenesis of PD (increased the β-arrestin2 levels restored the anti-inflammation of Drd2 in α-Syn-induced inflammation –  to read more about this).
  • New research suggests that AMBRA1 regulates the removal of old/sick mitochondria (mitophagy) via a novel pathway that is independent of Parkinson’s-associated PINK1 & PARKIN – a new target in developing therapies for PD? ( to read more about this).
  • Contact between the endoplasmic reticulum (where protein is made in a cell) & Mitochondria (the power station) is a hot topic in Parkinson’s at the moment. New research suggests interaction between PARKIN & Mitochondrial pro-fusion protein Mitofusin is required ( to read more about this).
  • In biology, enhancers are region of DNA that are bound by proteins to increase the likelihood of gene transcription. Recently researchers found enhancers active in dopamine neurons that link genetic variation to specific conditions, including Parkinson’s ( to read more about this).
  • Nuclear receptor related 1 protein (NURR1) is a protein that appears to be critical for dopamine neuron survival. New biorxiv manuscript identifies kinase inhibitors that regulate (increase or decrease) NURR1 activity. Implications for Parkinson’s? ( to read more about this).

  • Myristoylated alanine-rich C kinase substrate (or MARCKS) reflects degeneration at the early stage of Alzheimer’s. New research finds similar changes in MARCKS in Parkinson’s mouse & postmortem human brains ( to read more about this).
  • New study looks at the regional differences in Parkinson’s-associated Leucine-rich repeat kinase 2 (LRRK2) mRNA. “Predominant form of LRRK2 mRNA is full length, with shorter isoforms present at a lower copy number” ( to read more about this).
  • An interesting genetic analysis of variants in ATP13A2, PLA2G6 and FBXO7 genes in a cohort of Chinese individuals with early-onset Parkinson’s. Results indicate PLA2G6 & ATP13A2 may contribute to EOPD susceptibility in Chinese population, but not FBXO7 ( to read more about this).
  • New research suggests that senescence of glial cells (not neurons) in the brain drives dementia in a mouse model of Tau dependent neurodegenerative disease. Implications for Parkinson’s? ( to read more about this).
  • A population‐based cohort study of 2,544,748 Swedes, born 1920 to 1950 finds that “High job demands appear to increase PD risk in men, especially in men with high education”. High job control raised risk in lower educated ( to read more about this).

  • Interesting new connections being made between Parkinson’s-associated PINK1 & PARKIN proteins and the biology underlying motor neuron disease/amyotrophic lateral sclerosis ( to read more about this).
  • As induced pluripotent stem cells (iPSCs) are being taken to the clinic for Parkinson’s, researchers assess cross-site reproducibility in iPSC-based experiments and find that it is poor. They propose solutions ( to read more about this).
  • Further evidence of Parkinson’s-associated alpha-synuclein protein spreading through neural circuits in a prion-like fashion. Apparently botulinum toxin B blocked the spread by inactivating the synaptic vesicle fusion machinery ( to read more about this).
  • Loss of Parkinson’s-associated PARKIN could contribute to an impairment of the ability of mitochondria (the power stations of the cell) to handle calcium (PARKIN directly participates in the selective regulation of MICU1 and, indirectly, MICU2) ( to read more about this).
  • New research suggests that the syntaxin 17 (a mitochondria‐associated membrane protein) plays pivotal roles in mitochondrial division & Parkinson’s-associated PINK1/Parkin‐mediated mitophagy (disposal of mitochondria –  to read more about this).
  • Does the measuring of protein mis-folding of proteins like Parkinson’s-associated alpha synuclein affect the protein? Interesting question & potential solution explored in this report ( to read more about this).
  • Further high-magnification analysis of Parkinson’s-associated alpha synuclein finds a particularly stable toxic form of the protein (called Meta-αS-Os) could perhaps be considered as a principal target to control the amyloidogenesis & its pathogenesis ( to read more about this).
  • Parkinson’s-associated protein PINK1 does not regulate basal platelet mitophagy & is dispensable for platelet function. Subtle enhancements of activation-induced reactive oxygen species were detected ( to read more about this).

  • Deubiquitinating enzyme ubiquitin-specific peptidase 14 (USP14) has been shown to modulate waste disposal in cells (both proteasome activity & autophagy). New study finds USP14 can rescue PINK1/Parkin-disrupted fly model of Parkinson’s (
  • Young adult mice with Parkinson’s-associated LRRK2-G2019S genetic variants are MORE resilient to a depression-like syndrome resulting from chronic social stress ( to read more about this).
  • Large screening study of modifiers (druggable genes) of Parkinson’s-associated alpha synuclein levels finds 60 promising targets. 6 genes (ACSBG1, CHMP4B, DCLK1, DUSP11, KDELR2 & LGALS3BP) get characterised in cell lines, flies, mice, & human neurons ( to read more about this).
  • A comparison of normal, A53T, & A30P alpha synuclein protein finds that only A53T α-syn exhibit postsynaptic dysfunction, inducing tau dependent postsynaptic impairment – implications for Parkinson’s? ( to read more about this).
  • Researchers assess altered DNA regulation (methylation of promoters) of 5 Parkinson’s-associated genes (SNCA, PRKN, PINK1, DJ-1 & LRRK2) in 3 regions of postmortem brain, & find differences (in substantia nigra in some CpG dinucleotides –  to read more about this).
  • Interesting new experimental epigenetic-based approach for Parkinson’s using CRISPR-dCas9 technology to reduce levels of alpha synuclein (rescues SNCA triplication hiPSC-derived dopaminergic neurons –  to read more about this).


Disease mechanism

  • Silencing of the class II transactivator (CIITA) – a transcriptional co-activator required for MHCII induction – is effective in reducing the neuroinflammation & neurodegeneration observed in a mouse model of Parkinson’s ( to read more about this).
  • Pre- or post-treatment of Vitamin D helps to protect dopamine neurons against neuroinflammation & oxidative stress in rodent model of Parkinson’s ( to read more about this).
  • Removal of a gene called Kir6.2 exerts the protective effect on dopamine neurons in a mouse model of Parkinson’s. Kir6.2 knockout suppressed the excessive iron accumulation in the neurotoxic model. Regulating Kir6.2 may be a promising strategy for PD ( to read more about this).
  • Researchers
  • have published data suggesting that experimental Parkinson’s treatment Ursodeoxycholic Acid (UDCA) improves mitochondrial function & redistributes Drp1 in skin cells (fibroblasts) from people with Alzheimer’s ( to read more about this and click here for the press release).

  • Aged mice with Parkinson’s-assocaited G2019S LRRK2 genetic variant are more prone to develop alpha synuclein toxicity than normal aged mice. Aging is appeared to be a major determinant of G2019S LRRK2 associated α-synucleinopathy & loss of dopamine neurons ( to read more about this).
  • An IL-4 neutralizing antibody significantly increased survival of dopamine neurons in a rodent model (LPS) of Parkinson’s by inhibiting microglial activation & production of proinflammatory markers ( to read more about this).
  • Degeneration & impairment of melanopsin-containing retinal ganglion cells in the eye may affect to sleep & circadian dysfunction that are reported in Parkinson’s. Could protection or stimulation may lead to better quality of life? ( to read more about this).
  • MMP-2200 reduces Parkinson’s-associated dyskinesia. NMDA receptor antagonist MK-801 is anti-dyskinetic, but also pro-parkinsonian. MMP-2200 + MK-801 together reduce L-DOPA-induced dyskinesia (MMP-2200 does suppress the pro-parkinsonian activity of MK-801 –  to read more about this).
  • New brain imaging technique (diffusion MRI) found to be useful in primate models of Parkinson’s ( to read more about this).
  • Mitochondria help to buffer transient calcium elevations & prevent cell death induced by calcium overload. Now researchers show that mitochondrial calcium homeostasis is disrupted in fly models of Parkinson’s (including LRRK2) & restoration is beneficial ( to read more about this).

  • A transient post-translational modification hints at a new function for Parkinson’s-associated DJ-1 protein – it could serve as a signal for sensing oxidant stress ( to read more about this).
  • The ENIGMA consortium has a manuscript on bioRxiv indicating that there is a positive genetic association between the surface area of the cerebral cortex of the brain & Parkinson’s ( to read more about this).
  • The CHARGE Consortium also has a manuscript on biorxiv indicating that genetic variations determining volume & surface area of the cerebral cortex have been previously associated with conditions like Parkinson’s & Alzheimer’s ( to read more about this).
  • Researchers report that LGK974 – a PORCUPINE inhibitor – reduced the cell death in a model of Parkinson’s by interfering with the WNT/β-CATENIN pathway & reducing mitochondrial proapoptotic release ( to read more about this).
  • Prexton therapeutics (being acquired by Lundbeck) has published preclinical primate results for Foliglurax (aka PXT002331), a novel positive allosteric modulator of the metabotropic glutamate receptor 4 being developed as a treatment for Parkinson’s. The results suggest that Foliglurax can “alleviate the motor symptoms of Parkinson’s and the motor complications induced by L‐dopa [dyskinesias] in primates. PXT002331 is the first compound of its class to enter phase IIa clinical trials” ( to read more about this).

  • Dynactin – a protein involved in transporting cargo along microtubules – is found to be present in Parkinson’s-associated Lewy bodies (with alpha synuclein), but it is NOT present in multiple systems atrophy inclusions ( to read more about this).
  • Researchers report on the ability of brain imaging agent, BF-227, to bind to Parkinson’s-associated alpha synuclein & they suggest that compounds based on fluorobenzoxazoles may offer an approach to obtaining an α-Syn imaging agent ( to read more about this).
  • Meta analysis of 15 studies suggests that use of nonsteroidal anti-inflammatory drugs was not associated with the risk of Parkinson’s ( to read more about this).
  • Injection of alpha synuclein (pSer129) into the mouse brain results in accelerated accumulation of retinal alpha synuclein in the eye. Could Raman spectroscopy be used to differentiate a PD vs. healthy retina? ( to read more about this).
  • Further evidence of Montelukast exerting a neuroprotective effect in a neurotoxic model of Parkinson’s (reducing microglial activation –  to read more about this).
  • Administration (for 1–2 weeks) of traditional herbal medicine ‘Honokiol’ beginning 7 days after neurotoxin delivery, reduced behavioural impact in a model of Parkinson’s (by regulating PPARγ signaling –  to read more about this).

  • New study finds that even extremely low concentrations of Parkinson’s-associated alpha synuclein oligomers (a particular clustered combination the protein) can sensitize inflammatory responses (via TLR4) ( to read more about this).
  • New manuscript on BioRxiv suggests that mitochondrial function – measured in skin cells from 47 people with Parkinson’s – correlates with clinical severity. Useful biomarker for monitoring progression? ( to read more about this).
  • An analysis of alpha synuclein in skin cells from 15 people with Parkinson’s, 12 Lewy body dementia, & 12 multiple system atrophy (MSA) finds localization & load differences of aggregates may help to identify different pathogenesis among synucleinopathies ( to read more about this).
  • Researchers conduct a high-throughput screening study identifies a small molecule (called ‘SynuClean-D’) that is able to inhibit Parkinson’s associated-alpha synuclein aggregation ( to read more about this and click here for the press release).
  • researchers report that TP53 –Induced Glycolysis and Apoptosis Regulator (or TIGAR) protein is only present in substantia nigra Lewy bodies in Parkinson’s; not in cortical LBs & not present in other neurodegeneration-related inclusions ( to read more about this).
  • More evidence of Parkinson’s-associated protein LRRK2 being involved in lysosomal homeostasis. Implications for PD? Interesting that Rab7L1 – a candidate PD risk gene located within the PARK16 locus – is also involved in this process ( to read more about this).


Clinical research

  • An analysis of 106 electrode tracks in 53 patients finds that cognition is not influenced by deep brain stimulation electrode tracks passing through the caudate nucleus region of the brain ( to read more about this).
  • Analysis of inflammatory biomarkers in cerebrospinal fluid from 131 people with Parkinson’s, 27 PD with dementia (PDD), 24 with multiple system atrophy (MSA), 14 with progressive supranuclear palsy (PSP) & 50 controls found biomarkers were increased in PDD & MSA. The samples were part of the Swedish biofinder study. In Parkinson’s, higher levels of inflammatory biomarkers correlated with worse motor function & cognitive impairment indicating an association between inflammation & more aggressive disease course. Larger replication required ( to read more about this).
  • Interesting report of inability to replicate certain blood biomarkers between different sets of samples of people with de novo Parkinson’s – “highlights the importance of performing large-scale replication of findings from small index studies” ( to read more about this).


  • New report of machine learning being used to identify Alzheimer’s & Parkinson’s-related FDG-PET brain imaging patterns (classification algorithm was validated across four different datasets –  to read more about this).
  • New research suggests that ‘virtual footsteps‘ presented in an immersive, interactive Virtual Reality environment can significantly improve gait performance in people with Parkinson’s ( to read more about this).
  • 5 year study (Proactive and Integrated Management and Empowerment in Parkinson’s Disease – PRIME-PD) will see the implementation of a new integrated care model designed specifically for people with Parkinson’s. With generous Gatsby Foundation support, the study aims to bridge that gap by developing & evaluating a new model of proactive/integrated care that addresses the patients’ needs ( to read more about this).
  • Lysosphingolipid accumulation in the blood of people with glucocerebrosidase 1 (GBA1)-associated Parkinson’s points towards substrate reduction therapy ( to read more about this).
  • New research suggests that lower back pain occurs significantly more frequent in Parkinson’s (87.6%) compared to controls (62.6%); with longer duration & higher pain intensity ( to read more about this).

  • New research suggests limited to no association between appendectomy and increased risk of Parkinson’s, though in women, appendectomy for appendicitis, but not incidental appendectomy, was associated with a modestly elevated risk of PD ( to read more about this).
  • New method (HPLC-based) for the determination of L-dopa has been tested in a study exploring the impact of the ketogenic diet on the pharmacokinetics of L-dopa in Parkinson’s ( to read more about this).
  • Researchers present preliminary blood-based metabolomic data in support of potential association between traumatic brain injury (TBI) & Parkinson’s. Blood glutamic acid levels were higher in TBI & lower in PD groups compared to control levels ( to read more about this).
  • Apathy is common in prodromal Parkinson’s. Using neuroimaging in patients with REM sleep behaviour disorder, researchers show that apathy in this prodromal population is related to serotonin depletion in the dorsal raphe ( to read more about this).
  • Researchers highlight a new possibly pathogenic p.W378R GBA genetic variant in the Parkinson’s-associated GBA gene. They describe a 3‐generation family in which 8 members presented with PD & 3 with Gaucher’s disease ( to read more about this).
  • Genetic analysis (whole‐exome sequencing) of two independent cohorts of people with Parkinson’s (>1000 cases) finds that rare inherited variations in the pathway controlling mitochondrial DNA replication & repair influences the risk of Parkinson’s ( to read more about this).

  • New brain imaging study indicates increased connectivity in cortical sensorimotor areas (extending to the cerebello-thalamo-cortical pathway & parietal & frontal brain structures) in people with Parkinson’s on long-term L-dopa treatment ( to read more about this).
  • Vocal deficits during sustained phonations (‘aaah’ sounds )in people with LRRK2-associated Parkinson’s may be different to than those in people with idiopathic (spontaneous) PD ( to read more about this).
  • Researchers show that multimorbidity (the presence of two or more chronic medical conditions in an individual) is a small but significant predictor of quality of life in people with incident Parkinson’s ( to read more about this).
  • Almost half of the people with Parkinson’s who had colonic biopsies for this study had alpha-synuclein pathology in the colon, but no differences were observed in autonomic symptoms & testing between individuals with & without colonic neuropathology ( to read more about this).
  • urther examples of possible blood-based biomarkers for Parkinson’s. Exosomes are cell-derived bags of material that can be found in bodily fluids. APOA1 protein levels in exosomes is reduced as severity of PD increases ( to read more about this).
  • Visuospatial dysfunction is prevalent in PD & may affect gait. Researchers are planning an exploratory clinical study of visuospatial exploration & art therapy intervention in people with Parkinson’s. Here is what they are proposing ( to read more about this).
  • Interesting assessment of the occurrence of urinary symptoms in people with Parkinson’s who did not suffer from diseases known to influence the urinary function. Use of clinical and non-invasive urological assessment ( to read more about this).


Clinical trial news

  • Further delays for Acorda Therapeutics & their efforts to get their inhalable L-dopa product for Parkinson’s (called INBRIJA) approved by the FDA. The new review date of the NDA of INBRIJA has been moved from October 5, 2018 to January 5, 2019. ( to read more about this).

  • A 72 week randomized, double‐blind, multicenter trial of hydrogen water for Parkinson’s (178 participants) found no beneficial effect for drinking 1000ml/day H2 water in people with PD ( to read more about this).
  • Results from a phase 3, 26 week study of the MAO-B inhibitor Rasagiline as a monotherapy in recently diagnosed Parkinson’s suggest a significantly greater improvement in the MDS-UPDRS Part II + III compared to placebo ( to read more about this).
  • A 10 week clinical study of “Dance Therapy” suggest that psychotherapeutic movement intervention could be beneficial for folks with Parkinson’s ( to read more about this).
  • Researchers find consumer grade smartphones can be used to accurately separate not only people with idiopathic REM sleep behavior disorder (iRBD – thought to be a precursor to PD) from controls, but also iRBD from Parkinson’s ( to read more about this).

  • Bioelectron Technology Corp‘s drug EPI-589 – which is being clinically tested in Parkinson’s – has been found to be safe & well tolerable in people with Amyotrophic Lateral Sclerosis/motor neurone disease in Phase IIa clinical testing (Click here to read more about this).
  • A randomized, controlled pilot study of the effects of vitamin D supplementation on balance in Parkinson’s finds that short term, high dose vitamin D supplementation appears safe in people with PD, but did not significantly improve balance ( to read more about this).
  • A 3-month study of aerobic exercise training (stationary cycle) has a significant positive impact on the general upper limb functions (capacity to draw lines) in people with Parkinson’s ( to read more about this).


Other news

  • Yumanity Therapeutics – a biotech focused on therapies to treat neurodegeneration – today announced that its lead clinical candidate, YTX-7739, is entering IND-enabling studies for the treatment of Parkinson’s. First-in-human studies to start in Q4 2019 ( to read more about this).

  • The US_FDA gave Nuplazid (Pimavanserin) a clean bill of health for the treatment of Parkinson’s psychosis. “Analysis finds no new or unexpected safety risks associated with” the treatment ( to read more about this).


Review articles/videos

  • A lot of Parkinson’s-related research attention is being focused on the pedunculopontine nucleus as a consequence of its connection to the control of gait & its role in levodopa-insensitive gait symptoms of PD. New review provides an excellent overview ( to read more about this).
  • Interesting review linking the unfolded protein response to inflammation & depression – implications for Parkinson’s? ( to read more about this).
  • Interesting review of Parkinson’s: Biomarkers, Treatment, and Risk Factors (Click here to read more about this).
  • Interesting perspective asking if Parkinson’s could result from corticostriatal activity acting as a “stressor” for nigrostriatal terminals, ultimately driving retrograde nigrostriatal degeneration? ( to read more about this).
  • Interesting review of the role the common stomach bacterium Helicobacter pylori could play in Parkinson’s – interesting piece of data: People with PD are 1.5-3-fold more likely to be infected with H. pylori than people without PD ( to read more about this).

  •  Interesting comment about not wasting the ‘Golden Year’ in Parkinson’s. “At a minimum, let the patient know that there are early PD disease modifying trials being conducted and they may want to seek information” ( to read more about this).
  • A nice review/update of the genetics of Parkinson’s. “A growing number of reported genes described as causal genes (DNAJC13, TMEM230, GIGYF2, HTRA2, RIC3, EIF4G1, UCHL1, and CHCHD2) are still awaiting replication” ( to read more about this).
  • Fascinating review of the role of brain vasculature in neurodegenerative disorders, like Parkinson’s & Alzheimer’s – a much neglected aspect of research, but many commonalities between conditions ( to read more about this).
  • Really interesting review of experimental therapeutic strategies for Parkinson’s that way beyond dopaminergic drugs – discussing the challenges associated with the development of novel therapies. Sadly not open access ( to read more about this).
  • A lot of attention in Parkinson’s is focused on the chemical dopamine. Recently, there has been a shift towards another chemical affected by PD: norepinephrine. This is a nice review discussing the mechanisms by which it & α-syn pathology could affect PD ( to read more about this).
  • The National Institute for Health and Care Excellence published updated guidelines on managing Parkinson’s in 2017. This is a commentary discusses the implications of the guidance 4 healthcare professionals involved in the care of people with PD ( to read more about this).


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

And there it is, just some of the highlights from September 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 October!


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.

4 thoughts on “Monthly Research Review – September 2018

    1. Simon may have been a bit too modest to announce that award himself. I would certainly agree from my own experience that he has “had a significant impact on the lives of people with Parkinson’s and/or involved people with Parkinson’s in a participatory way in their work.”


    2. Hi Daniel,
      Gad you liked the post. I hope you got home ok from the Grand Challenges/Rallying meeting in Grand Rapids – it was very nice to meet you and thanks again for the book.
      The award was wholly unexpected and took me completely by surprise. I was lost for words. I was honored to be mentioned in the same sentence as Prof Bas Bloem, let alone to be sharing an award with him. It meant a lot that the community voted for me and I was deeply touched.
      Kind regards,


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