Evidence map›Paper›PMID 42834215›Full record

ReviewReviews of physiology, biochemistry and pharmacology2027

AA and Parkinson's Disease.

Undurti N Das

Abstract readReview
PubMed Publisher
In one paragraph

Review in Reviews of physiology, biochemistry and pharmacology, 2027. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Undurti N DasUND Life Sciences, Battle Ground, WA, USA.ORCID https://orcid.org/0000-0002-0191-9508

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is due to degeneration of dopaminergic neurons in substantia nigra pars compacta. PD neuropathology is characterized by the presence of Lewy bodies that contain aggregated α-synuclein, which has been implicated in a range of interactions with phospholipid membranes and free fatty acids. I propose that α-synuclein interacts with arachidonic acid (AA) to regulate the function of dopaminergic neurons. α-Synuclein sequesters AA, whereas AA induces the formation of oligomers that are alpha-helical; resistant to fibril formation; more prone to disaggregation, enzymatic digestion, and degradation; and hence less likely to cause neuronal damage and induce PD. In addition, AA interacts with syntaxin to regulate exocytosis of various neurotransmitters, including dopamine. AA has potent anti-inflammatory actions, serves as a mechanotransducer, influences cell membrane fluidity, enhances glucose uptake by neurons, possesses cytoprotective action, and is the precursor of anti-inflammatory lipoxin A4 (LXA4), actions that maintain the integrity of dopaminergic neurons in the substantia nigra pars compacta. The dynamic equilibrium among α-synuclein, syntaxin, AA, exocytosis of dopamine, formation of LXA4, and the inflammatory process is involved in the development of PD. This implies that deficiency of AA can render dopaminergic neurons susceptible to inflammatory neurodegeneration and development of PD. Hence, it is proposed that administration of AA and DHA (that are present in substantial amounts in the brain) can be used in the prevention and management of PD.

Indexed as

Arachidonic AcidParkinson Diseasealpha-SynucleinAnimalsDopamineDopaminergic NeuronsExocytosisHumansQa-SNARE Proteinsalpha-SynucleinArachidonic AcidDopamineQa-SNARE ProteinsExocytosisFibrilLewy bodiesParkinson’s diseaseSyntaxinα-Synuclein

Identifiers

PMID42834215

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.