Developing a Cure for Alzheimer's: New Clues on the Role of Tau

Development of a cure for Alzheimer's disease will ultimately depend on a better understanding of the chain of events that leads to progressive death of brain cells. Scientists have long recognized the pathological hallmarks of AD: amyloid plaques and neurofibrillary tangles.

Joseph V. Campellone, MD

Division of Neurology, Cooper Union Hospital, Camden, NJ

Thursday, May 3, 2007; 3:00 PM 

 

Affecting an estimated 4 1/2 million people in the United States, Alzheimer's disease (AD) is expected to become a growing medical, social, and economic concern as our elderly population expands. It is expected that AD will exert an increasing burden on all aspects of society as the number of patients affected by AD will only continue to increase. The most common cause of dementia, an effective cure for AD remains elusive.

Current treatments are limited to improving symptoms, yet lack the ability to stop disease progression. Several cholinesterase inhibitors are available, which improve cognitive function by improving communication between surviving brain cells. These include Aricept (donepezil), Exelon (rivastigmine) and Reminyl (galantamine).

Another medication, memantine, also improves cognitive function and may also have some protective effect. Nonetheless, patients treated with any of these medications eventually exhibit relentless decline in function.

Development of a cure will ultimately depend on a better understanding of the chain of events that leads to progressive death of brain cells. Scientists have long recognized the pathological hallmarks of AD: amyloid plaques and neurofibrillary tangles. The presence of these abnormal structures in the brains of Alzheimer's patients has stirred debate as to whether these accumulations cause injury to brain cells or are just an indicator that something is wrong. Recently, most attention has been directed towards amyloid. Several genetic mutations affecting amyloid protein itself or proteins that process amyloid have been identified to result in Alzheimer's disease.

The recent demonstration that reducing tau protein improves outcome in an animal model of Alzheimer's disease provides a new target for preventing cell death. The persistence of amyloid plaques in these affected animals without cognitive decline offers more evidence that amyloid may not in itself be toxic to neurons. As investigators also observed reduced likelihood for seizures in these animals, it may be that tau protein disorders serve as a common mediator for cell injury in other conditions as well, both acute and chronic. It will be exciting to see what role tau protein plays in other neurologic diseases and whether this information can be translated into effective treatment for human disease.

Read Related News: Strategy Could Put Breaks on Alzheimer's

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