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RESEARCH UPDATE 2004

Aging, Alzheimer's and Other Neurodegenerative Disorders

Rachel Neve

For many years, Alzheimer's disease (AD) research has focused on either beta-amyloid plaques, protein fragments derived from the amyloid precursor protein (APP) that accumulate in brains with AD, or fibrous tangles, as the two potential causes. Rachael Neve, PhD, director of the Mailman Research Center's Molecular Neurogenetics Laboratory, has proposed a new theory, suggesting that the cause is the toxicity of APP itself. Her research shows that a peptide called C99, derived from APP, invades neurons and causes them to try to divide. Since neurons cannot divide, this attempt at entering the cell cycle forces the neurons to self-destruct. This is a whole new way of looking at Alzheimers disease and suggests the illness looks like cancer. Unlike cancer, however, in which cells divide uncontrollably, neurons die because they cant divide. Neves research was honored by the Alzheimer's Research Forum during the 2003 Society for Neuroscience annual conference for her courage in putting forth original alternative explanations to broaden the Alzheimer's disease field.

Harper and Dorsey

Harper and Dorsey

Alzheimer's and Insomnia

David Harper, PhD, and investigators in the Geriatric Psychiatry Research Program have been collaborating with Cynthia Dorsey, PhD, director of the Sleep Research Laboratory, in an effort to improve the quality of life for individuals with Alzheimer's disease (AD). Many of these elderly individuals suffer from insomnia or fragmented sleep patterns. Among findings to date are that individuals with AD have delayed peaks of both activity and body temperature rhythms, compared to healthy elderly men and women. These findings point to an abnormality in the area of the brain known to control the circadian rhythms of the body and suggest that altering body temperature may improve sleep in those with AD.

Anne Cataldo

Alzheimer's disease (AD) ends in damage to much of the brain, but the disease process starts decades earlier, in individual nerve cells. Researchers in the Mailman Research Center's Molecular Neuropathology Laboratory, directed by Anne Cataldo, PhD, have found that unusually large compartments which process proteins, including a protein fragment called Ab that accumulates in the brains of individuals with AD, are one of the first signs of the disease. These experiments may lead to enhanced early detection and ultimately, to preventive treatment of Alzheimer's disease.

Ole Isacson

Led by Ole Isacson, Dr Med Sc, scientists in the Mailman Research Center's Neuroregeneration Laboratory have shown that mouse embryonic stem cells can become dopamine nerve cells capable of restoring lost function in animal models of Parkinsons disease. These same researchers are also using neuroprotective drugs to fight such neurodegenerative diseases as Alzheimer's, Huntington's and Parkinson's. These novel methods deliver cells and substances to the brain to bolster resistance to illness. Basic research, such as this, may lead to therapies that could delay, stabilize or even reverse the course of debilitating brain disorders.