Alzheimer's disease (AD) is the leading cause of dementia worldwide and since age is the most significant risk factor for the disease, the incidence of AD is expected to triple to over 100 million affected by 2050.  The amyloid hypothesis of AD states that the accumulation of the toxic amyloid-� peptide (A�) induces neuronal dysfunction, leading to brain atrophy, dementia and death.  Several therapeutic modalities have been pursued intending to reduce the A� burden in AD brain including inhibition of synthesis, acceleration of clearance and disruption or inhibition of aggregation.  Recent data from clinical trials addressing each of these modalities will be reviewed, with a view towards anticipating the results of ongoing clinical studies in order to provide a sense of when the amyloid hypothesis might be fully tested.  A brief overview of tau dysfunction in AD will be provided and the current status of tau approaches and therapeutics will be summarized.  Finally the status and challenges of symptomatic approaches will be reviewed.

Current and future prospects for novel therapeutics for Alzheimer's disease

243rd National Meeting (2012)

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