Neural Protein May Stop the Progression of Alzheimer Disease

By Phelps, Jerry | Environmental Health Perspectives, January 2005 | Go to article overview

Neural Protein May Stop the Progression of Alzheimer Disease


Phelps, Jerry, Environmental Health Perspectives


Stein TD, Anders N J, DeCarli C, Chan SL, Mattson MP, Johnson JA. 2004. Neutralization of transthyretin reverses the neuroprotective effects of secreted amyloid precursor protein (APP) in APPSW mice resulting in tau phosphorylation and loss of hippocampal neurons: support for the amyloid hypothesis. J Neurosci 24:7707-7717.

As many as 4.5 million Americans suffer from AIzheimer disease (AD), which usually begins after age 60, and the risk of developing the disease goes up with age. About 5% of men and women aged 65-74 have AD, and nearly half of those aged 85 and older have the disease.

AD is characterized by the presence of protein plaques and tangles of fibers in brain tissue. The disease may in fact be caused by the abnormal processing of the so-called amyloid precursor protein and the accumulation of the protein [beta]-amyloid. Other brain abnormalities in people with AD include nerve cell death in specific areas that are vital to memory and other mental abilities, as well as lower levels of certain neurotransmitters. A recent study by NIEHS grantee Jeffrey Johnson of the University of Wisconsin-Madison has identified a protein known as transthyretin that blocks the effects of [beta]-amyloid.

In working with a transgenic mouse containing defective human genes associated with early-onset AD, Johnson and colleagues noticed that although these mice had high levels of [beta]-amyloid, they did not exhibit any neurodegenerative symptoms. …

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