The first study demonstrates that the application of pbm is cable of altering the microbiome in people with parkinsons disease.

https://www.linkedin.com/feed/update/urn:li:activity:6884757119929864192/

 

Taking the information from the screen shoot reference above, I would like to present for our "Educating Doctors" a brief.

Microbiome Changes in Humans with Parkinson’s Disease after Photobiomodulation Therapy: A Retrospective Study
SymByx Adelaide clinical trial

https://www.mdpi.com/2075-4426/12/1/49/pdf​

Participants were treated with a four-diode laser device (904 nm, 30 mW) transdermally over nine points of the abdomen in a grid pattern (3.6 joules per point, 32.4 joules total energy) and over the C1/C2 region of the neck (7.6 joules total energy) as well as transcranially with four LED diodes (240 joules total energy) and intranasally with a single LED diode (15 joules total energy). Total treatment time was 30 min.

Participants were treated three times per week for 4 weeks, followed by twice per week for 4 weeks and then once per week for 4 weeks (24 total treatments). The treatment protocol used Class 1 lasers and LEDs, with no need for safety glasses.

Generated sequences were analysed for metagenomic bacterial diversity using the Quantitative Insights into Microbial Ecology 2 (QIIME2).

Microbiome community structure was analysed using alpha diversity (within sample richness) and beta diversity (between sample similarity), calculated using the q2-diversity plug-in at a rarefaction of 30,000 sequences sampling depth.

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Stacked bar chart indicating the relative abundances of phyla detected in the gut microbiomes of PD participants before (pre-) and after 12 weeks (post-) of PBM treatment. A = pre-treatment; B = post-treatment.​

Our study showed potential capable of altering the microbiome in individuals with Parkinson’s disease, specifically it produced favourable changes in gut microbiome diversity in a patient undergoing radiotherapy and immunotherapy for breast cancer, with an increase in the number of known beneficial bacteria and a decrease in the number of potentially pathogenic genera.

 

When we look for potential mechanisms of action, how about a pathogen?

Microbial BMAA and the Pathway for Parkinson’s Disease Neurodegeneration

https://www.frontiersin.org/articles/10.3389/fnagi.2020.00026/full
https://sci-hub.se/10.3389/fnagi.2020.00026​

The neurotoxin β-N-methylamino-L-alanine (BMAA) is a natural non-proteinogenic diamino acid produced by several species of both prokaryotic (cyanobacteria) and eukaryotic (diatoms and dinoflagellates) microorganisms.


The “neurotoxin hypothesis” for sporadic neurodegenerative diseases such as Parkinson’s disease (PD). Chronic intestinal exposure to β-N-methylamino-L-alanine (BMAA) may trigger neurodegeneration by promoting protein misfolding, mitochondrial dysfunction and innate immune responses in genetically susceptible individuals, initially in the enteric nervous system (ENS) and later in the central nervous system (CNS) through retrograde transport via the vagus nerve.

Cyanobacteria are photoautotrophic bacteria, a nonphotosynthetic clade of divergent cyanobacteria named Melainabacteria was identified in groundwater, tap water, wastewater treatment plants and also as members of the human gut microbiota.

Regular exposure to dietary sources of this microbial neurotoxin may drive protein misfolding and mitochondrial dysfunction with concomitant activation of innate immune responses, chronic low-grade gut inflammation, and ultimately the neurodegenerative features observed across the gut-brain axis in Parkinson’s disease (PD).​

Sensing and responding to UV-A in cyanobacteria

https://pubmed.ncbi.nlm.nih.gov/23208372/​

Motile cyanobacteria use a very precise negative phototaxis signaling system to move away from high levels of solar radiation, which is an effective escape mechanism to avoid the detrimental effects of UV radiation. Recently, two different UV-A-induced signaling systems for regulating cyanobacterial phototaxis were characterized at the photophysiological and molecular levels.


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Of course, the idea of damaging cyanobacteria is a bad thing according the authors.

We know the gut is an anaerobic "dark" environments for bacteria. Is it possible that a mechanism of action is UV-A-induced photo-toxicity to cyanobacterial?

 

My aunt has Parkinson's - never went into the sun - woke up at noon, played on the computer till midnight, rinse repeat...

 

this study suggests b alanine reduces anxiety whilst also affecting BDNF in the hippocampus of rats. https://pubmed.ncbi.nlm.nih.gov/30803507/

 

Dysbiosis also disrupts tryptophan metabolism, shifting the balance of serotonin and kynurenine pathways. A disturbed kynurenine pathway has been linked to Parkinson's, cardiovascular disease, multiple sclerosis, amyotrophic lateral sclerosis (ALS), and other neurological diseases.

There is a particularly strong link between the microbiome and Parkinson's disease, where constipation suffered by a majority of Parkinson's disease sufferers is linked to α-synuclein accumulation in the enteric nervous system, increased intestinal permeability (leaky gut), and local inflammation (increased pro-inflammatory cytokines), which can occur years before the neural symptoms of Parkinson's disease become apparent.