# # # # 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 July 2022. The post is divided into 10 parts based on the type of research: Top 5 pieces of Parkinson’s news Articles of general interest Basic biology Disease mechanism Clinical research New clinical trials Clinical trial news Conferences/lectures Other news Review articles/videos # # # #

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So, what happened during July 2022?

In world news:

July 8th – Former Prime Minister of Japan Shinzo Abe was assassinated while giving a public speech in the city of Nara, Japan.

 

July 11th – The first operational image (Webb’s First Deep Field) from the technologically amazing James Webb Space Telescope was presented to the public. The image revealed the galaxy cluster SMACS 0723 – a cluster of galaxies about 4 billion light years from Earth (everything about this project excites me – especially Trappist 1):

July 28 – The Commonwealth Games began in Birmingham, England.

 

July 28th – DeepMind announced that their AlphaFold tool has determined the structures of almost every protein (around 200 million proteins) – just one year after releasing data on the first 20,000 proteins. The freely available 23-terabyte database represents “the beginning of a new era of digital biology” – click here to read more about this)

July 30th – Billionaire Bill Gates increased his commitment to Alzheimer’s research (Click here to read more about this)

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

In July 2022, there were 894 research articles added to the Pubmed website with the tag word “Parkinson’s” attached (7,103 for all of 2022 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. Is alpha synuclein ‘interferon’ with the immune response?:

Researchers reported that Parkinson’s-associated α-synuclein is required for neuronal expression of interferon-stimulated genes (in response to viral infection). Curiously, when neurons that do not have α-synuclein are treated with type 1 interferon, they failed to induce a broad range of interferon stimulated genes, suggesting that α-synuclein interacts with type 1 interferon signaling. In addition, interferon-mediated phosphorylation of STAT2 is also dependent on α-synuclein. The researchers also looked at postmortem brain tissue from people with Parkinson’s (Click here to read more about this & click here to read an OPEN ACCESS version of the report).

2. Treadmills, PPARα, and fenofibrate:

Researcher reported that treadmill exercise reduced the spread of α-synuclein aggregation pathology in aged genetically engineered (A53T) mice. They determined that this effect resulted from the activation of Peroxisome proliferator-activated receptor alpha (PPAR-α) which stimulated lysosomal biogenesis (via TFEB). Interestingly when the researchers treated mice with fenofibrate – a PPARα agonist – in the absence of exercise, it also reduced α-synuclein aggregation pathology (Click here to read more about this).

 

3. Does Yerbe mate matter?

A multicenter case-control study across 3 countries (Argentina, Paraguay, & Uruguay) found an association between Yerba mate tea concentration per serving and lower risk of developing Parkinson’s (Click here to read more about this and click here to read a SoPD post on the topic).

4. Astrocytes to the rescue:

Researchers reported that astrocytes can alleviate Parkinson’s-related α-synuclein pathology by regulating a series of the proteostasis procedures (involving formation, transmission, disaggregation, & clearance of aggregates) both in vitro & in vivo. In addition, transplantation of healthy midbrain astrocytes into a Parkinson’s mouse model reduced α-synuclein pathology and protected the dopamine neurons from neurodegeneration (Click here to read more about this and click here for the associated editorial).

 

5. PD-associated protein affects communication within cells:

Disturbed contacts between intracellular structures like the endoplasmic reticulum & mitochondria is affected in some cases of Parkinson’s. Now researchers have reported that a protein called “cysteine-rich with EGF-like domain (Creld)” regulates ER-mitochondria communication. Creld is “a poorly characterized risk gene for PD”, but loss of this protein led to mitochondrial hyperfusion and reduced oxidation in various models (Click here to read more about this).

 

Articles of general interest

• The World Health Organisation highlights 6 “workable avenues” to address global disparities in Parkinson’s (Click here to read more about this); The 6 avenues for action involve domains of:
  – Disease burden
  – Advocacy & awareness
  – Prevention & risk reduction
  – Diagnosis, treatment, & care
  – Caregiver support
  – Research
• Please take some time to complete this survey and help shape clinical trial participation experience, if you are someone with Parkinson’s who has or hasn’t taken part in research, they would love to hear from you (Click here to read more about this).
• Wonderful interview with Prof Anders Bjorklund of Lund University – a pioneer & expert in cell replacement strategies for Parkinson’s – “Be open-minded, proactive, & open to sharing experience, knowledge, & information” (Click here to read more about this).

• Some beautiful (& hard) insights in a new paper exploring transitions & challenges for people with Parkinson’s & their families; A qualitative study; “I’ve been very lucky. I had a lovely wife, I’ve got lovely children. I’ve got lovely friends. What more can you want?” (Click here to read more about this).
• LivedHealth have a great set of short videos addressing questions about Parkinson’s; Lots of experts providing advice on numerous topics:

 

Basic biology news

• Researchers report p21-activated kinase 4 (PAK4) as a key regulator of Parkinson’s-associated α-synuclein aggregation; Postmortem PD brain reveals an inverse correlation between PAK4 activity & α-synuclein aggregation; LOF & GOF in vivo experiments support (Click here to read more about this)
• New research identifies VCP/p97 as a target for SMER28 & presents compounds that activate the D1 ATPase activity of VCP/p97 enhancing both autophagic & proteasomal neurotoxic protein clearance (Click here to read more about this).
• More evidence that Parkinson’s-associated LRRK2 kinase activity modulates GCase levels & enzymatic activity, across complementary models; Results point towards cell-type-specific effects (Click here to read more about this).

• Researchers report rβ2-subunit alternative splicing stabilizes Cav2.3 Ca2+ channel activity during continuous midbrain dopamine neuron-like activity; Data “imply a potential (patho)physiological role of β-subunit alternative splicing” in Parkinson’s (Click here to read more about this).
• Heparin induces Parkinson’s-associated α-synuclein to form new fibril polymorphs with attenuated neuropathology; New study provides the structural mechanism for how, & emphasizes the important role of biological polymers (Click here to read more about this).
• So much interesting research being published at the moment on less-studied proteins associated with Parkinson’s: Researchers present in situ architecture of the lipid transport protein VPS13C at ER–lysosome membrane contacts (Click here to read more about this).
• Regulators of the Parkinson’s-associated LRRK2 signaling pathway including vps35 & PPM1H converge upon causing centrosomal deficits; Enhanced LRRK2 kinase activity impacts these events to alter the normal biology of a cell (Click here to read more about this).
• New research finds that Parkinson’s-associated α-Synuclein fibrils formed in the presence of different divalent cations have distinct structural & cytotoxic features (in vitro – click here to read more about this).

• New research reports synaptic location is a determinant of the detrimental effects of α-Synuclein pathology to glutamatergic transmission in the basolateral amygdala (Click here to read more about this).
• Useful tool – researchers present a versatile fluorescence-quenched substrate (LysoFQ-GBA) for quantitative measurement of glucocerebrosidase activity within live cells; Validated using different cell types with various GBA status & GCase inhibitors (Click here to read more about this).
• New research explored mammalian target of rapamycin (mTOR) signaling in dopamine neurons. It revealed importance of mTORC1/2 signaling on structure & function of dopamine neurons (Click here to read more about this).
• TWNK encodes for the mitochondrial twinkle helicase, essential for mtDNA replication. New research finds TWNK variants in patients with Parkinson’s or parkinsonism, with or /out signs of myopathy. Data “strengthen the relation between the TWNK gene & PD” (Click here to read more about this).
• Researchers used confocal & super-resolution microscopy, subcellular fractionation, & electron microscopy of immunogold-labeled α-synuclein preformed fibrils to demonstrate rapid internalization & targeting directly to lysosomes (in as little as 2 min); “While a portion of preformed fibrils remain in lysosomes for a long period, a smaller portion are transferred to naive cells along with markers of multivesicular bodies” – further work needed to address relationship between internalized PFFs & their influence on endogenous α-synuclein (Click here to read more about this).

• New data proposes that Tau may act downstream of α-synuclein pathology to affect neuronal homeostasis & survival in α-synucleinopathies, like Parkinson’s; Loss of Tau significantly delays onset of deficits in the TgA53T in vivo & PFF in vitro models (Click here to read more about this).
• The neuropeptide neurotensin is expressed in the midbrain & induces Long-Term Depression (LTD) of D2R synaptic currents, but the source of neurotensin is not known. Now researchers report neurotensin is released from dopamine neurons themselves (Click here to read more about this).
• Loss of the mitochondrial enzyme glutamate pyruvate transaminase 2 (GPT2) causes early neurodegeneration in locus coeruleus (Click here to read more about this).
• Researchers report that Parkinson’s-associated LRRK2-G2019S perturbs mitochondrial homeostasis & reprograms cell death pathways in macrophages; Pivotal role for GSDMD (promoting switch to RIPK-dependent necroptosis – click here to read more about this).
• Could stress granules be the origin of neuromelanin granules (NG) in the substantia nigra? Data allows for cautious hypothesizing that stress granules form in close proximity to NGs, possibly due to the oxidative stress caused by neuromelanin-bound metals (Click here to read more about this).
• New research finds “dopamine signaling in the nucleus accumbens core has a causal role in novelty-based learning in a way that cannot be predicted based on purely associative factors” (Click here to read more about this).

• Cholinergic interneuron inhibition potentiates corticostriatal transmission in direct medium spiny neurons & rescues motor learning in mouse model of Parkinsonism; Control exerted on corticostriatal transmission depends on the integrity of dopamine inputs (Click here to read more about this).
• New tool – researchers generate nanobodies that preferentially bind to Parkinson’s-associated α-synuclein fibrils, but not α-synuclein monomers; Potential for “therapeutic development in α-synuclein-related pathogenesis”? (Click here to read more about this).
• α-Synuclein V15A variant in familial Parkinson’s exhibits weaker lipid-binding properties; It displays “a reduced affinity for phospholipids & increased propagation activity compared with wild-type” in vitro; Plus data from 2 independent Japanese families (Click here to read more about this).
• Cell type matters: Researchers report that the influence of Parkinson’s-associated noncoding variations on LRRK2 expression is specifically propagated through microglia; Inflammation as a causal factor for PD? Does this generalise to G2019S? (Click here to read more about this).
• In a new biorxiv manuscript, researchers examine LRRK2 protein-protein interactome across 15 tissue-specific interactomes; High degree of similarity for LRRK2 interactors in putamen, caudate & nucleus accumbens (Click here to read more about this).

 

Disease mechanism

• New research reports how a small molecule Toll-like receptor antagonist (NPT1220-312 – Neuropore Therapies) can rescue α-synuclein fibril pathology in models of Parkinson’s (Click here to read more about this).

• New research demonstrates that re-routing metabolism by the mitochondrial pyruvate carrier inhibitor MSDC-0160 can attenuate neurodegeneration in a rodent model (unilateral 6-OHDA) of Parkinson’s (Click here to read more about this).
• New research introduces NXP031 – a new compound consisting of Aptamin C & Vitamin C – which is neuroprotective against Parkinson’s-associated α-synucleinopathy; It blocked propagation of aggregated α-Syn in vivo (mice) by alleviating oxidative stress (Click here to read more about this).
• Adeno-associated virus 9-mediated gene delivery of Nurr1 & Foxa2 ameliorates symptoms & pathologies of…. an Alzheimer’s mouse model (by suppressing neuro-inflammation & glial pathology); Improved memory & cognitive function (Click here to read more about this).
• Reduction of α-synuclein pathology in a mouse model of Parkinson’s, using a brain-penetrating bispecific antibody; “RmAbSynO2-scFv8D3” (mmm, catchy name) targets aggregated α-synuclein & binds to the transferrin receptor for facilitated CNS uptake (Click here to read more about this).
• Dopamine receptor agonist Pramipexole inhibits astrocytic NLRP3 inflammasome activation (via Drd3-dependent autophagy) in a mouse model of Parkinson’s (Click here to read more about this).

• Researchers from Ossianix Inc present a single domain shark antibody targeting the transferrin receptor 1 that delivers a TrkB agonist antibody to the brain & provides neuroprotection in model of Parkinson’s (Click here to read more about this).
• CSF-derived extracellular vesicles from patients with Parkinson’s – administered intranasally to healthy mice – induce symptoms & “unconventional” pathology months later: α-synuclein aggregations in the red nucleus, premature gray hair, & astrogliosis (Click here to read more about this).
• Researchers explore Fingolimod-induced proteome changes in the cerebellum & frontal cortex and report that the drug’s effects on the brain are mediated through biochemical modulation of bioenergetics, autophagy & neuroinflammatory networks (Click here to read more about this).
• New biorxiv manuscript reports USP30 inhibition induces mitophagy & reduces oxidative stress in Parkinson’s-associated parkin-deficient & CCCP-stressed human iPSC-derived neurons (Click here to read more about this).
• New research explores in rodents how glutamatergic mechanisms in the inferior colliculus influence motor control, classically attributed to the basal nuclei circuitry, could be useful in the development of new therapeutics to treat Parkinson’s (Click here to read more about this).

• Bimodal regulation of axonal transport by the GDNF-RET signaling axis; A divergence in the response of primary motor neurons to GDNF vs cell lines; GDNF-RET inhibition rescues transport deficits in ALS mice (SOD1G93A); Implications for Parkinson’s? (Click here to read more about this).
• New research identifies the mechanism of action of selective orally bioavailable chaperone-mediated autophagy activators (with favorable brain exposure); Stabilization of RARα & N-CoR1; Implications for Parkinson’s? I am curious to learn more about Selphagy Therapeutics…. (Click here to read more about this).
• Very short therapeutic window of opportunity for nicotine in a fly model of Parkinson’s; “May help to explain the lack of efficacy of nicotine in human clinical trials”… what ever happened to the NIC-PD clinical trial results??? (Click here to read more about this).
• New research used multi-parameter high-throughput screen for cytoplasmic:nuclear translocation of endogenous TFEB & related transcription factor TFE3; They identify AKT inhibitors & quinazoline-derivative compounds (Click here to read more about this).
• New research presents pharmacological chaperones for GCase that switch conformation with pH enhance enzyme levels in Gaucher in vivo models; Opportunity for Parkinson’s? (Click here to read more about this).

Clinical research

• New research provides qualitative insights into the patient experiences of early-stage Parkinson’s; A mixed methods analysis is used to identify cardinal features for clinical trial outcome assessment (Click here to read more about this).
• New data finds “independent of presynaptic dopamine depletion, the thalamus is a major neural substrate for levodopa-induced dyskinesia & that a contracted thalamic shape at baseline is closely associated with an early development of LID” in Parkinson’s (Click here to read more about this).
• Olfactory swab sampling optimization for α-synuclein aggregate detection in patients with Parkinson’s; “Combining the CSF results with the results of nasal swab can increase the diagnostic accuracy to nearly 100%” (Click here to read more about this).

• Researchers attempt to develop a fully automatic video-based hypomimia (facial bradykinesia) assessment tool & estimate the prevalence & characteristics of hypomimia in de-novo Parkinson’s cases (Click here to read more about this).
• Scientists report clinical & structural brain correlates of hypomimia in early-stage Parkinson’s, using data from COPPADIS study database; “Reduced facial expressivity in PD is related to severity of symptoms of apathy” (Click here to read more about this).
• Using multiparametric quantitative MRI, researchers report spatial gradients in the putamen & caudate nucleus “that were robust across individuals, clinical conditions, & datasets”, particularly in Parkinson’s (Click here to read more about this).
• Using PPMI 2010 to 2018 data, researchers report CSF neurofilament heavy levels “may be useful in stratifying patients with Parkinson’s who have different progression rates”; N=404; High baseline cNfH= higher MDS-UPDRS Part-III & faster decreases in MoCA (Click here to read more about this).

• Could blood hexosylsphingosine be a marker for Parkinson’s linked with GBA1 genetic variants? Answer: Maybe “mild” variants, but needs more research (Click here to read more about this).
• New research tested the performance of the “PREDIGT Score” in the DeNoPa & PPMI studies (N=563 newly diagnosed Parkinson’s cases & 306 controls; “Results reveal a robust performance” (Click here to read more about this).
• Researchers report glycosphingolipid changes in plasma in Parkinson’s independent of glucosylceramide levels; Findings indicate a broader shift in lipid homeostasis; GSLs changes more evident in the male PD cohort (Click here to read more about this).
• New study suggests association between height & substantia nigra p/ compacta neuron density in cases of Lewy body dementia (N=14) or Parkinson’s (N=22) compared to controls (N=19), supporting previous research linking short stature & increased risk of PD (Click here to read more about this).

• Imaging from 1,941 PD cases finds incidentally-discovered white matter disease was associated with subsequent Parkinson’s; Association strengthened with younger age & increased white matter disease severity; Covert brain infarction=not associated with PD (Click here to read more about this).
• Researchers explore associations of cognitive dysfunction with motor & non-motor symptoms in patients with de novo Parkinson’s, & find different relationship patterns (Click here to read more about this).
• New paper employs short & long read genetic sequencing analysis for the Gaucher & Parkinson’s-associated GBA gene; They confirm that GBA variants are more common in Lewy body dementia than in PD, + CNVs are relatively common (Click here to read more about this).
• New research presents monocyte profiles that provide an “early” & unique biomarker strategy for tracking clinical immune-based interventions; Data from their sargramostim studies; Requires validation in larger studies (Click here to read more about this).

• α-synuclein seed amplification in CSF & brain from patients with different brain distributions of pathological α-synuclein in the context of co-pathology & non-Lewy Body Dementia diagnoses (Click here to read more about this).
• Researchers at report direct interactions between Parkinson’s-associated a-Synuclein & Rab3a (in solution & on lipid membranes using NMR spectroscopy); a-Syn is an inhibitor of Rab3a GTP hydrolysis (Click here to read more about this).
• “Voxel-based diktiometry”: all the cool kids are doing it! New study combines convolutional neural networks with voxel-based analysis & applies it in diffusion tensor imaging for Parkinson’s; Highlights cerebellum & brain stem white matter areas (Click here to read more about this).
• Large-scale nationwide cohort of 6.9M individuals aged ≥40 years who underwent the Korean National Health Screening during 2009, finds waist circumference & abdominal obesity were associated with increased Parkinson’s risk (HR 1.16 (95% CI, 1.10–1.23 – click here to read more about this).

• Longitudinal PET imaging of presynaptic terminals in early Parkinson’s; DAT-based imaging showed robust 2-year decline in early PD, but SV2A-based imaging did not; DAT imaging “did not correlate with clinical motor progression” (N=27 PD + 18 controls – click here to read more about this).
• Identifying & characterising sources of variability in digital outcome measures in Parkinson’s; New paper introduces “a conceptual framework to assist clinical research teams investigating a specific Concept of Interest within a particular Context of Use” (Click here to read more about this).
• The Parkinson’s Study Group SURE-PD3 Investigators use longitudinal item response theory analysis to reanalyze outcomes from their Phase 3 trial; They find faster progression in the tremor domain than the non-tremor domain before levodopa treatment; “We suggest that in neurological diseases with distinct impairment domains, clinical or anatomical, this application may identify patterns of change unappreciated by standard statistical methods” (Click here to read more about this).
• Plasma biomarkers of inflammation & vascular injury are associated with cognitive decline & could be useful in prognosis of cognitive decline in patients with mild cognitive impairment (Click here to read more about this).

• Further data on the use of plasma neuronal extracellular vesicles: New research indicates their potential use as biomarkers to inform cognitive prognosis in Parkinson’s; Low α-syn & Tau + impaired insulin signaling may underlie cogitive impairment (Click here to read more about this).
• Could a certain type of personality be a prodromal marker for idiopathic rapid eye movement sleep behavior disorder (which is a prodromal stage in some cases of Parkinson’s)? (Click here to read more about this).
• Assessment of hand grip strength & anthropometry (systematic measurement of the physical properties) in 75 cases of Parkinson’s at diagnosis finds sex specific associations between various variables & the level of P-cortisol (Click here to read more about this).
• More data from Roche on the reliability & validity of their Parkinson’s Mobile Application (v1 & 2) for remote monitoring of early PD; The new gold standard for everyone to use? (Click here to read more about this).

• Gut microbiota analysis based on fecal samples from 20 monozygotic twins (N=40) discordant for Parkinson’s finds minimal differences in bacterial taxa abundance at species level (Click here to read more about this).
• The glucocerebrosidase (GBA) genetic variant T369M is not a risk factor for Parkinson’s in Swedish cohorts (Click here to read more about this).
• The Movement Disorder Society has provided an update of the treatment guidelines for invasive therapies in the treatment of Parkinson’s; “Should only be used for appropriately selected patients, but in those can profoundly change the lives of people with PD” (Click here to read more about this).
• The study protocol for the SMARTSPEECH study has been published – investigating the use of a smartphone application to investigate speech biomarkers of Parkinson’s & other synucleinopathies over a period of 2 years (Click here to read more about this).

 

New clinical trials

• They had me with “BUTTER” – A new clinical trial registered: Small Phase I pilot study (N=10; 30 days) exploring the short-chain fatty acid (SCFA) prodrug tributyrin as a potential therapy for persons with Parkinson’s (The BUTTER study – Click here to read more about this).
• New clinical trial registered: “Amped-PD”: Amplifying physical activity through music in Parkinson’s; N=44; 6-week community-based, self-directed walking program (Click here to read more about this).

 

Clinical trial news

• Kainos Med announces that their US Phase 2 clinical trials for their FAF inhibitor KM-819 in Parkinson’s will begin in August; After optimal dose finding, 288 participants will be randomly assigned (Click here to read more about this).
• Annovis gets the nod from US FDA for their Phase 3 clinical study of Buntanetap (Posiphen) in individuals recently diagnosed with Parkinson’s to proceed; 6 months; double-blind, placebo-controlled; 2 doses; N=450; Primary endpoint = UPDRS II+III OFF (Click here to read more about this).

Conferences/lectures

• The 2022 Edinburgh Parkinson’s Lecture will be held on 28th Sept 2022 and will be given by Dr Julie Jones of Robert Gordon University (Aberdeen). The lecture is entitled “The Importance of Exercise for People with Parkinson’s: Evidence, Empowerment and Enablement” (Click here to read more about this).

• “Planning for Parkinson’s Prevention: A trial design forum” – really interesting hybrid conference in October focused on the next generation of clinical trials focused on actual prevention of PD – Boston, Oct 2nd & 3rd 2022 (Click here to read more about this).
• The Grand Challenger in Parkinson’s conference will be held on September 28th & 29th. The topic for this year’s meeting is Modifying Progression — From Molecules to Trials, and it will highlight recent advances that may fuel development of therapies to slow or stop disease progression (Click here to read more about this).

 

Other news

• The study rationale & protocol for multiple N-of-1 trials to investigate hypoxia therapy in Parkinson’s; This “evaluation of hypoxia therapy could provide insight in novel pathways that may be pursued for PD treatment” (Click here to read more about this).
• ZyVersa has been awarded a grant from the Michael J Fox Foundation to explore if ‘IC 100’, a CNS-penetrating monoclonal ASC (inflammasome) Inhibitor, can block neuroinflammation in models of Parkinson’s (Click here to read more about this).
• SERG Technologies – a startup focused on optimising care for neurodegenerative movement disorders – has raised £1.6m to continue development of its platform technology for the continuous monitoring & treatment optimisation of Parkinson’s (Click here to read more about this).

• EpicentRx has been awarded a grant from the Michael J Fox Foundation to evaluate the therapeutic potential of RRx-001 – a direct NLRP3 inflammasome inhibitor – in models of Parkinson’s (Click here to read more about this).
• Kyowa Kirin axes their new Parkinson’s medication – KW-6356, which is a follow-up to their first-generation adenosine A2 antagonist – saying development and regulatory hurdles are too daunting Parkinson’s (Click here to read more about this).
• Parkinson Canada (partnered with the Davis Phinney Foundation) have published the latest edition of the Every Victory Counts® manual, creating a resource with the information Canadians need to live well with Parkinson’s (Click here to read more about this).

Review articles/videos

And there it is, just some of the highlights from July 2022 – 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 August!!!

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You can do whatever you like with it!

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EDITOR’S NOTE: The author of this post is an employee of Cure Parkinson’s, so he might be a little bit biased in his views on research and clinical trials supported by the trust. That said, the trust has not requested the production of this post, and the author is sharing it simply because it may be of interest to the Parkinson’s community.

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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