Letter to the editor

Schwartz, Roberta Hanfling

doi:10.1016/j.mehy.2004.01.016

Cited by 4 publications

(1 citation statement)

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“…Although low-protein diets are known to aid levodopa control of PD symptoms by evening out variations in brain levodopa levels (a post-prandial surge in plasma branched-chain amino acids following a protein-rich meal competitively inhibits brain levodopa uptake), what is proposed here is that such diets might aid prevention or slow progression of PD by boosting striatal Parkin levels [269][270][271]. Although the impact of plant-based diets on rate of PD progression has not been assessed clinically, a few anecdotal reports, published or online, are consistent with benefit in this regard [272,273]. The impact of low-protein diets on striatal Parkin/PINK1 expression and progression of neuronal loss could readily be studied in rodent PD models.…”

Section: Keeping Mitochondria Efficient By Optimizing Mitophagy-h 2 Smentioning

confidence: 74%

Nutraceuticals Targeting Generation and Oxidant Activity of Peroxynitrite May Aid Prevention and Control of Parkinson’s Disease

McCarty

Lerner

2020

IJMS

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Parkinson’s disease (PD) is a chronic low-grade inflammatory process in which activated microglia generate cytotoxic factors—most prominently peroxynitrite—which induce the death and dysfunction of neighboring dopaminergic neurons. Dying neurons then release damage-associated molecular pattern proteins such as high mobility group box 1 which act on microglia via a range of receptors to amplify microglial activation. Since peroxynitrite is a key mediator in this process, it is proposed that nutraceutical measures which either suppress microglial production of peroxynitrite, or which promote the scavenging of peroxynitrite-derived oxidants, should have value for the prevention and control of PD. Peroxynitrite production can be quelled by suppressing activation of microglial NADPH oxidase—the source of its precursor superoxide—or by down-regulating the signaling pathways that promote microglial expression of inducible nitric oxide synthase (iNOS). Phycocyanobilin of spirulina, ferulic acid, long-chain omega-3 fatty acids, good vitamin D status, promotion of hydrogen sulfide production with taurine and N-acetylcysteine, caffeine, epigallocatechin-gallate, butyrogenic dietary fiber, and probiotics may have potential for blunting microglial iNOS induction. Scavenging of peroxynitrite-derived radicals may be amplified with supplemental zinc or inosine. Astaxanthin has potential for protecting the mitochondrial respiratory chain from peroxynitrite and environmental mitochondrial toxins. Healthful programs of nutraceutical supplementation may prove to be useful and feasible in the primary prevention or slow progression of pre-existing PD. Since damage to the mitochondria in dopaminergic neurons by environmental toxins is suspected to play a role in triggering the self-sustaining inflammation that drives PD pathogenesis, there is also reason to suspect that plant-based diets of modest protein content, and possibly a corn-rich diet high in spermidine, might provide protection from PD by boosting protective mitophagy and thereby aiding efficient mitochondrial function. Low-protein diets can also promote a more even response to levodopa therapy.

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Section: Keeping Mitochondria Efficient By Optimizing Mitophagy-h 2 Smentioning

confidence: 74%

Nutraceuticals Targeting Generation and Oxidant Activity of Peroxynitrite May Aid Prevention and Control of Parkinson’s Disease

McCarty

Lerner

2020

IJMS

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Postmortem brain fatty acid profile of levodopa-treated Parkinson disease patients and parkinsonian monkeys

Julien

Berthiaume²,

HadjTahar

et al. 2006

Neurochemistry International

102

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The intestinal luminal sources of α-synuclein: a gastroenterologist perspective

Lerner

2021

Nutrition Reviews

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Parkinson’s disease is characterized by nonmotor/motor dysfunction, midbrain dopaminergic neuronal death, and α-synuclein (aSN) deposits. The current hypothesis is that aSN accumulates in the enteric nervous system to reach the brain. However, invertebrate, vertebrate, and nutritional sources of aSN reach the luminal compartment. Submitted to local amyloidogenic forces, the oligomerized proteins’ cargo can be sensed and sampled by a specialized mucosal cell to be transmitted to the adjacent enteric nervous system, starting their upward journey to the brain. The present narrative review extends the current mucosal origin of Parkinson’s disease, presenting the possibility that the disease starts in the intestinal lumen. If substantiated, eliminating the nutritional sources of aSN (eg, applying a vegetarian diet) might revolutionize the currently used dopaminergic pharmacologic therapy.

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Letter to the editor

Cited by 4 publications

References 0 publications

Nutraceuticals Targeting Generation and Oxidant Activity of Peroxynitrite May Aid Prevention and Control of Parkinson’s Disease

Nutraceuticals Targeting Generation and Oxidant Activity of Peroxynitrite May Aid Prevention and Control of Parkinson’s Disease

Postmortem brain fatty acid profile of levodopa-treated Parkinson disease patients and parkinsonian monkeys

The intestinal luminal sources of α-synuclein: a gastroenterologist perspective

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