More evidence from experiments on mice on how and why exercise is good for People with Parkinson’s (PwPs):
The popularized article: Link between exercise and dopamine
And from the abstract and significance statement of the original (non-open access) article:
Physical exercise improves motor performance in individuals with Parkinson’s disease and elevates mood in those with depression. Although underlying factors have not been identified, clues arise from previous studies showing a link between cognitive benefits of exercise and increases in brain-derived neurotrophic factor (BDNF). (emphasis added).
and:
Exercise has been shown to improve movement and cognition in humans and rodents. Here, we report that voluntary exercise over 30 days leads to an increase in evoked dopamine (DA) release throughout the striatum, and an increase in BDNF in the dorsal (motor) striatum. The increase in DA release appears to require BDNF, indicated by the absence of DA release enhancement with running in BDNF+/- mice. Activation of BDNF receptors using a pharmacological agonist was also shown to boost DA release. Together these data support a necessary and sufficient role for BDNF in exercise-enhanced DA release, and provide mechanistic insight into the reported benefits of exercise in individuals with dopamine-linked neuropsychiatric disorders, including Parkinson’s disease and depression. (emphasis added).
The citation:
Voluntary exercise boosts striatal dopamine release: evidence for the necessary and sufficient role of BDNF, Guendalina Bastioli, Jennifer C. Arnold, Maria Mancini, Adam C. Mar, Begoña Gamallo-Lana, Khalil Saadipour, Moses V. Chao, Margaret E. Rice,Journal of Neuroscience 16 May 2022, JN-RM-2273-21; DOI: 10.1523/JNEUROSCI.2273-21.2022
So that covers why exercise is good for all. But what about what is good for the one?
… there is growing recognition that PD is not a single entity but instead reflects multiple diseases, in which different combinations of environmental, genetic and potential comorbid factors interact to direct individual disease trajectories… The clear consequence of there being distinct diseases that collectively form PD, is that there is no single biomarker or treatment for PD development or progression. We propose that diagnosis should shift away from the clinical definitions, towards biologically defined diseases that collectively form PD, to enable informative patient stratification. N-of-one type, clinical designs offer an unbiased, and agnostic approach to re-defining PD in terms of a group of many individual diseases. . (emphasis added).
The citation links to PubMed where you can download the full article, should you be so inclined. The next citation also links to an open access free article.
In this article, Riggare reports on self tracking done in 2012 (as a Person with Parkinson’s), and the offer the possibility that self-tracking of symptoms and medications can help to inform the physician’s decisions over the course of treatment. In other words, one should be a self-advocate as a patient and work with your physician to achieve the best combination of treatments to address Parkinson’s and its comorbidities. (At least that’s my takeaway from the article. Others might differ).
Another look at PD aims to categorize it into various sub-types:
This article is a “desk review”of other studies, using specific criteria to either include/exclude each study in the results. Their conclusion:
Conclusion: Subtyping studies undertaken to date have significant methodologic shortcomings and most have questionable clinical applicability and unknown biological relevance. The clinical and biological signature of PD may be unique to the individual, rendering PD resistant to meaningful cluster solutions. New approaches that acknowledge the individual-level heterogeneity and that are more aligned with personalized medicine are needed. (emphasis added).
Among the articles cited in the bibliography is this one (another open access article):
In this, the authors describe their methodology and results from the Oxford cohort (one of several cohorts of PwPs and controls that have been used for research. (I would take the time and effort to locate the original publication describing the different cohorts involved in the effort to find biomarkers, but I am currently experiencing a wave of Parkinson’s related apathy. Check my past posts, or do a search on PubMed – I do remember that Oxford and Boston were two of the cohorts of PwPs. But I digress).
Results: Apolipoprotein A1 and C-reactive protein levels differed across our PD subtypes, with severe motor disease phenotype, poor psychological well-being, and poor sleep subtype having reduced apolipoprotein A1 and higher C-reactive protein levels. Reduced apolipoprotein A1, higher C-reactive protein, and reduced vitamin D were associated with worse baseline activities of daily living (MDS-UPDRS II).
Conclusion: Baseline clinical subtyping identified a pro-inflammatory biomarker profile significantly associated with a severe motor/nonmotor disease phenotype, lending biological validity to subtyping approaches. No blood biomarker predicted motor or nonmotor prognosis. © 2019 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society. (emphasis added).
In other words: Close, but no cigar. But I, for one, certainly could have benefited from this knowledge had it been available 60 years ago. (don’t get me started – I’ve played that tape many times before).
Oh well, let’s end on a high note:
bob's brain: living well with a movement disorder and other comorbidities 