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Alzheimer Disease - Therapeutic Strategies (Paperback, Softcover reprint of the original 1st ed. 1994)
Loot Price: R1,471
Discovery Miles 14 710
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Alzheimer Disease - Therapeutic Strategies (Paperback, Softcover reprint of the original 1st ed. 1994)
Series: Advances in Alzheimer Disease Therapy
Expected to ship within 10 - 15 working days
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Since the apoE4 allele is a risk factor or susceptibility gene in
late-onset familial and sporadic AD, the mechanism of disease
expression may involve metabolic effects that are isoform specific.
Isoform-specific interactions of apoE therefore become critical in
the mechanism of AD pathogenesis. Detailed characterization of the
binding of the apoE isoforms with proteins and peptides relevant to
the pathology of the disease may be critical in understanding
disease pathogenesis. These critical isoform-specific interactions
of apoE may involve interactions with proteins and pep tides in the
defining neuropathologic lesions of the disease, the
neurofibrillary tangle and senile plaque. Other possible critical
isoform-specific interactions include the mechanism of
internalization, intracellular trafficking, and subsequent
metabolism. In addition, differential post-translational
modifications of apoE isoforms may determine differences in
metabolism contributing to the pathogenesis of the disease.
Oxidation of apoE may confer several isoform-specific,
biochemically distinct properties. Since {3A peptide binds apoE in
the lipoprotein binding domain of the protein and not in the
receptor-binding domain, apoE could target bound {3A4 peptide to
neurons via the LRP receptor. Internalization of the apoEI {3A
peptide complex into the cell, by the same route as the
apoE-containing lipoproteins, would result in incorporation into
primary lysosomes and pH dependent dissociation. The demonstration
of apoE in the cytoplasm of neurons, with isoform-specific
interactions of apoE with the microtubule-binding protein tau
demonstrated in vitro, suggest additional, testable hypotheses of
disease pathogenesis.
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