QBI Neuroscience Seminar: Alzheimer’s disease: Aβ amyloid is the critical target for primary (pre-AD) and secondary (preclinical) disease-modifying strategies
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- Professor Colin L Masters, Head of the Neurodegeneration Division,
The Florey Institute, Laureate Professor, The University of Melbourne
Alzheimer’s disease: Aβ amyloid is the critical target for primary (pre-AD) and secondary (preclinical) disease-modifying strategies.
Abstract: There are two basic forms of Alzheimer’s disease (AD). The common (>95%) form is sporadic, and is caused by the failure to clear the Aβ peptide (mean age at onset 80 years). The rare (< 5%) autosomal dominant familial form is caused by the over-production of this peptide (mean age at onset 45 years). In both forms, the kinetics of Aβ accumulation are similar, taking about 30 years to accumulate approximately 10mg of Aβ. Thus we estimate that sporadic AD starts about the age of 50 years and the autosomal dominant form starts about 15 years of age. A disease modifying strategy will be needed to keep the total brain Aβ burden close to normal levels (<2.5 mg) and prevent/delay onset of both forms. Such a strategy may encompass lowering production, stabilizing / neutralizing the toxic Aβ species, and promoting it’s clearance from the brain. Interventions targeting Aβ in the earliest / mildest stages of the natural history of AD are beginning to show efficacies.
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