By Philip M. Parker
In March 2001, the nationwide Institutes of well-being issued the subsequent caution: "The variety of sites supplying health-related assets grows on a daily basis. Many websites offer precious info, whereas others could have info that's unreliable or misleading." moreover, as a result quick raise in Internet-based details, many hours will be wasted looking out, identifying, and printing. on the grounds that merely the smallest fraction of knowledge facing Alzheimer ailment is listed in se's, similar to www.google.com or others, a non-systematic method of web learn may be not just time eating, but additionally incomplete. This booklet used to be created for doctors, scholars, and individuals of most people who are looking to behavior clinical learn utilizing the main complex instruments to be had and spending the smallest amount of time doing so.
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In March 2001, the nationwide Institutes of future health issued the next caution: "The variety of websites supplying health-related assets grows on a daily basis. Many websites offer worthwhile details, whereas others could have details that's unreliable or deceptive. " additionally, as a result swift elevate in Internet-based info, many hours will be wasted looking, picking, and printing.
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Additional resources for Alzheimer Disease - A Bibliography and Dictionary for Physicians, Patients, and Genome Researchers
Suite 160 Tampa, Fl 33612 Timing: Fiscal Year 2006; Project Start 01-APR-1997; Project End 30-JUN-2011 Summary: (provided by applicant): This Program Project Grant is focused on understanding physiological and biochemical alterations in the brain underlying changes in cognition during aging and Alzheimer's disease. There are several themes that weave throughout the Program Project. A major theme is to examine the role of oxidative stress and inflammation in aging. There are 2 major sources of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in the brain and these are from the glia (primarily the microglia) and the mitochondrion.
CoQ10 is a cofactor of the electron transport gene, which has strong antioxidant properties. It is extremely well tolerated in human subjects and is under clinical development for treatment of Parkinson's Disease, Huntington's Disease and amyotrophic lateral sclerosis. We will also look at the effects of L-iminoethyl-L-lysine, which is a relatively specific inhibitor of NOS2. We will determine whether treatment with either CoQ10 or L-NIL can exert neuroprotective effects against beta-amyloid deposition and oxidative damage, and improve memory in transgenic mouse models of AD.
In this application we propose to use a variety of neuropsychological, neurological and imaging tools to examine the earliest stages of AD and to follow these subjects throughout their lives. At death a comprehensive neuropathologic examination will be performed and the clinical, radiological and pathological views of the disease correlated. Tissues and DNA obtained from these subjects will be available for research on the biology and genetics of the disease. Individual research projects within the ADRC will examine various aspects of the cellular and molecular biology of AD as well as an in-depth analysis of brain function in 28 Alzheimer Disease human subjects using MRI.
Alzheimer Disease - A Bibliography and Dictionary for Physicians, Patients, and Genome Researchers by Philip M. Parker