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2 defective proteins conspire to impair the nerve cell's 'powerhouse' in Alzheimer's disease
Date:5/13/2011

ieve that changes in the brains of Alzheimer patients begin years or even decades before the signs of Alzheimer disease become apparent.

"By the time the cells are dead, it's far too late to do much," said Johnson, who is also a professor in the Department of Pharmacology and Physiology and a scientist in the Center for Neural Development and Disease. "Therefore, in the field of Alzheimer research, investigators are looking for early markers and indicators of disease so that patients could be identified before significant nerve cell death has occurred. In addition, studies in many labs are ongoing to identify treatments that could target these early events.

"Perhaps," Johnson adds, "the new information on mitochondrial dysfunction in Alzheimer disease can be used to fight the disease, as it is likely an important target for therapeutic intervention. Given the fact that Alzheimer disease is a very complex disease, a monotherapeutic approach may not be as effective as a combinatorial treatment strategy, as is the case for treating other diseases including cancer and diabetes. Further studies on why and how mitochondria are compromised in Alzheimer disease as well as other neurodegenerative conditions are needed to develop effective treatments which will increase mitochondrial function and improve the health of the brain cells."


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Contact: Tom Rickey
tom_rickey@urmc.rochester.edu
585-275-7954
University of Rochester Medical Center
Source:Eurekalert

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