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Fibrillar plaque diseases

Just like in coiled-coils, p-sheet secondary structure (Fig. 2) is ubiquitous in natural examples and in proteins and biomaterials. Alzheimer s disease is characterized by fibrillar amyloid plaques in the cerebral parenchyma. The insoluble amyloid fibrils are predominantly formed upon conformational switching of the 42 amino acid... [Pg.146]

Abundant neuritic plaques and neurofibrillary lesions define Alzheimer s disease. Plaques are extracellular deposits made of the fibrillar P-amyloid peptide. The paired helical filament (PHF) makes up the bulk of the intraneuronal neurofibrillary pathology of Alzheimer s disease, with the straight filament (SF) being a minority species. [Pg.752]

Lesions of Alzheimer s disease, evident as dense plaques composed of fibrillar amyloid beta-proteins, likely develop when these proteins are first induced to form beta-sheet secondary structures. It was demonstrated that membranes containing oxidatively damaged phospholipids accumulated amyloid beta-protein significantly faster than membranes containing unoxidized phospholipids. The protein on oxidized membranes more readily changed conformation to a beta-sheet, indicating that oxidatively damaged phospholipid membranes... [Pg.341]


See other pages where Fibrillar plaque diseases is mentioned: [Pg.537]    [Pg.537]    [Pg.314]    [Pg.267]    [Pg.341]    [Pg.318]    [Pg.247]    [Pg.382]    [Pg.21]    [Pg.245]    [Pg.35]    [Pg.610]    [Pg.172]    [Pg.282]    [Pg.2430]    [Pg.422]    [Pg.62]    [Pg.205]    [Pg.147]    [Pg.260]    [Pg.250]    [Pg.102]    [Pg.280]    [Pg.300]   
See also in sourсe #XX -- [ Pg.536 ]




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