Publications by authors named "M S Mouradian"

Article Synopsis
  • * Researchers identified 38 genes that influence αSyn propagation, focusing on two genes, which help understand how αSyn interacts with lipids and forms inclusions resembling Lewy Bodies.
  • * Analysis of gene expression changes after manipulating these genes revealed a connection to increased risk variants in Parkinson's patients, supporting a model where genetic factors disrupt αSyn regulation, leading to disease progression.
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-Synuclein (-Syn) aggregation in Lewy bodies and Lewy neurites has emerged as a key pathogenetic feature in Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy. Various factors, including posttranslational modifications (PTMs), can influence the propensity of -Syn to misfold and aggregate. PTMs are biochemical modifications of a protein that occur during or after translation and are typically mediated by enzymes.

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Background: We aimed to assess how antimicrobial exposure affects Parkinson's disease (PD) risk.

Methods: A nested case-control study was performed to examine the association between antimicrobial exposure and newly diagnosed PD using the Clinical Practice Research Datalink (CPRD). Each PD case was matched by age, sex, and year of diagnosis (index date) to up to 15 controls.

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Neurodegenerative diseases encompass a heterogeneous group of disorders that afflict millions of people worldwide. Characteristic protein aggregates are histopathological hallmark features of these disorders, including Amyloid β (Aβ)-containing plaques and tau-containing neurofibrillary tangles in Alzheimer's disease, α-Synuclein (α-Syn)-containing Lewy bodies and Lewy neurites in Parkinson's disease and dementia with Lewy bodies, and mutant huntingtin (mHTT) in nuclear inclusions in Huntington's disease. These various aggregates are found in specific brain regions that are impacted by neurodegeneration and associated with clinical manifestations.

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