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| Year : 2009 | Volume
: 51
| Issue : 5 | Page : 56-60 |
Frontiers in the pathogenesis of Alzheimer's disease
Kumar Sambamurti1, KS Jagannatha Rao2, Miguel A Pappolla1
1 Department of Neurosciences, Medical University of South Carolina, 173 Ashley Avenue, BSB 403 Charleston, SC 29425
2 Department of Biochemistry and Nutrition, Central Food Technological Research Institute, Mysore - 570020, India
Correspondence Address:
Kumar Sambamurti
Department of Neurosciences, Medical University of South Carolina, 173 Ashley Avenue, BSB 403 Charleston, SC 29425.
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 21416019 
Alzheimer's disease (AD) is characterized by progressive dementia and brain deposits of the amyloid β protein (Aβ ) as senile plaques and the microtubule-associated protein, Tau, as neurofibrillary tangles (NFT). The current treatment of AD is limited to drugs that attempt to correct deficits in the cholinergic pathway or glutamate toxicity. These drugs show some improvement over a short period of time but the disease ultimately requires treatment to prevent and stop the neurodegeneration that affects multiple pathways. The currently favored hypothesis is that Aβ aggregates to toxic forms that induce neurodegeneration. Drugs that reduce Aβ successfully treat transgenic mouse models of AD, but the most promising anti-Aβ vaccination approach did not successfully treat AD in a clinical trial. These studies suggest that AD pathogenesis is a complex phenomenon and requires a more broad-based approach to identify mechanisms of neurodegeneration. Multiple hypotheses have been proposed and the field is ready for a new generation of ideas to develop early diagnostic approaches and develop successful treatment plans.
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