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beta-Amyloid protein aggregation: its implication in the physiopathology of Alzheimer's disease
L Dumery1, F Bourdel, Y Soussan
1UFR 927 des Sciences de la Vie, Université Pierre et Marie Curie, 4 Place Jussieu, 75252 Paris.
Abstract:
beta-Amyloid protein (A beta), a 39-42 residue peptide resulting from the proteolytic processing of a membrane-bound beta-amyloid precursor protein (APP), is one of the major components of the fibrillar deposits observed in Alzheimer patients. A beta fibril formation is a complex process which involves changes in A beta conformation and self-association to form cross-beta pleated sheets, protofibrils, and fibrils. Since the aggregation of soluble A beta peptide into fibrils is viewed as a critical event in the physiopathology of Alzheimer's disease (AD), preventing, altering, or reversing fibril formation may thus be of therapeutic value. This review will focus on the current state of knowledge of A beta fibril formation, with special emphasis on physiological and exogenous inhibitors which may have a therapeutic potential.
Insights
Beta-amyloid (A beta) fibril formation is central to Alzheimer's disease (AD) pathology. This review explores inhibitors of A beta aggregation, offering potential therapeutic strategies for AD.
Area of Science:
- Neuroscience
- Biochemistry
- Pathology
Background:
- Beta-amyloid (A beta) peptide, derived from amyloid precursor protein (APP), aggregates into fibrils.
- These fibrillar deposits are a hallmark of Alzheimer's disease (AD).
- A beta fibril formation involves conformational changes and self-association.
Purpose of the Study:
- To review the current understanding of A beta fibril formation.
- To highlight physiological and exogenous inhibitors of A beta aggregation.
- To discuss the therapeutic potential of these inhibitors for Alzheimer's disease.
Main Methods:
- Literature review of studies on A beta aggregation and inhibition.
- Analysis of mechanisms underlying A beta fibril formation.
- Evaluation of identified inhibitors for therapeutic relevance.
Main Results:
- A beta aggregation is a complex process leading to pathological deposits.
- Various physiological and exogenous agents can inhibit A beta fibril formation.
- Inhibiting A beta aggregation is a promising therapeutic avenue for AD.
Conclusions:
- Understanding A beta fibril formation is crucial for developing AD treatments.
- Inhibitors of A beta aggregation hold significant therapeutic potential.
- Further research into these inhibitors could lead to effective AD therapies.