Findings in Alzheimer Disease Reported from Biomedical Research Institute of New Jersey (Nascent Ab42 Fibrillization In Synaptic Endosomes Precedes Plaque Formation In a Mouse Model of Alzheimer's-like B-amyloidosis).

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Zdroj: Genomics & Genetics Weekly; 4/5/2024, p639-639, 1p
Abstrakt: A recent study conducted by the Biomedical Research Institute of New Jersey has shed light on the accumulation of amyloid-beta peptide (Aß) aggregates in synapses, which may contribute to the synaptic loss seen in Alzheimer's disease (AD). The researchers found that Aß accumulates in synaptic compartments and is produced locally within endosomes, independent of the presence of amyloid plaques. They also identified the role of the protease endothelin-converting enzyme (ECE-1) in controlling the accumulation and fibrillization of nascent Aß in endosomes. This study provides valuable insights into the pathogenesis of AD and highlights potential therapeutic targets for the disease. [Extracted from the article]
Databáze: Complementary Index