PD needs paradigm shift: eg, Alzheimer's, HSV1, P. gingivalis, amyloid-beta and tau are antimicrobial peptides.

[aspergerian13]

Alzheimer's is experiencing a paradigm shift. Nonetheless, publicity about the important findings is seemingly nonexistent. This is somewhat akin to media silence about Costantini and HDT.

Here are Important findings about herpes, Alzheimer's, and dementia. Amyloid beta and Tau are antimicrobial peptides. Oodles of suppoting data. Quite exciting!

Massachusetts General announcement:

massgeneral.org/News/pressr...

Anti-herpetic Medications and Reduced Risk of Dementia in Patients with Herpes Simplex Virus Infections—a Nationwide, Population-Based Cohort Study in Taiwan : 2018.

ncbi.nlm.nih.gov/pmc/articl...

Corroboration of a Major Role for Herpes Simplex Virus Type 1 in Alzheimer’s Disease.

Ruth F. Itzhaki.

2018.

ncbi.nlm.nih.gov/pmc/articl...

Also:

Porphyromonas gingivalis in Alzheimer’s disease brains: Evidence for disease causation and treatment with small-molecule inhibitors.

ncbi.nlm.nih.gov/pmc/articl...

[jimcaster]

Interesting. More than 50% of the adult population has herpes simplex.

[aspergerian13 in reply to jimcaster]

APOE status is a variable.

[park_bear]

Indeed amyloid is a response to pathogens.

Appalling that $hundreds of millions have been wasted seeking to treat that instead of the cause.

[aspergerian13 in reply to park_bear]

Chronically treating symptoms has long been profitable. Thus it came to pass that avoiding cures became an operational method for medicationists and their Big Pharma overlords.

[LAJ12345]

ncbi.nlm.nih.gov/pmc/articl...

“ Cranberry and rice extracts interfere with gingipain activity and prevent the growth and biofilm formation of periodontopathogens.”

[aspergerian]

LAJ12345,

Excellent find. A friend's husband has Alzheimer's in which Gingivalis porphyromonas is likely to be significant.

[aspergerian13]

Citing cranberry gingipain 2014:

scholar.google.com/scholar?...

[felixned]

jvi.asm.org/content/90/6/2767

For your reading pleasure. I am 99% sure that when immuno therapy study is done 5 years and a billion dollars later we're going to be informed that alpha syN have secondary role in pd.

[aspergerian13 in reply to felixned]

I too would not be surprised.

[LAJ12345]

So do you think it is viruses and toxins doing the damage and the alpha syn is just the bodies way of entrapping the viruses? Perhaps the blobs of protein cause some of the symptoms by gumming up things but prevent the toxins doing more damage? So dissolving the protein clumps might rerelease the viruses and toxins into the body?

Doesn’t mannitol break down the protein clumps?

[aspergerian13]

You have sketched a possible scenario, probably one among several.

[aspergerian13]

Nice integration circa 2009:

Lewy body diseases are characterized by the presence of Lewy bodies, alpha-synuclein(AS)-positive inclusions in the brain. Since their main component is conformationally modified AS, aggregation of the latter is thought to be a key pathogenic event in these diseases.

The analysis of inclusion body constituents gives additional information about pathways also involved in the pathology of synucleinopathies.

Widespread mitochondrial dysfunction is very closely related to disease development. The impairment of protein degradation pathways, including both the ubiquitin-proteasome system and the autophagy-lysosome pathway also play an important role during the development of Lewy body diseases.

Finally, differential expression changes of isoforms corresponding to genes primarily involved in Lewy body formation point to alternative splicing as another important mechanism in the development of Parkinson’s disease, as well as dementia with Lewy bodies.

The present paper attempts to give an overview of recent molecular findings related to the pathogenesis of Lewy body diseases.

Molecular Pathology of Lewy Body Diseases.

Katrin Beyer, Montserrat Domingo-Sàbat, and Aurelio Ariza.

2009.

ncbi.nlm.nih.gov/pmc/articl...