Highlights include:
- new information about the biology of amyloid-ß, the main component in the amyloid plaques found in the brains of Alzheimer's disease patients, and where the field has concentrated its efforts for nearly 20 years
- the Tau Hypothesis, which suggests Alzheimer's disease is caused by abnormal chemical changes to tau proteins disrupting the normal cell biology of neurons
- the Oxidative Stress Hypothesis, which indicates neurons degenerate and die because the brains of patients with Alzheimer's disease have a disrupted oxidative metabolism leading to decreased neuronal energy supply and increased oxidative damage
- neuroimmunological hypotheses linking Alzheimer's disease to the chronic low level inflammation thought to underlie arthritis, coronary disease and other age-related conditions
- the development of biomarkers for early diagnosis
- new horizons for the development of anti-dementia drugs
Perry, ranked one of the top ten Alzheimer's disease researchers in the world in 2009, joined UTSA in 2006 from Case Western Reserve University, where he was a professor of pathology and neurosciences and the chair of Case Western Reserve's Department of Pathology. A prolific researcher, Perry is the second-most published Alzheimer's disease researcher, with 516 publications to his credit. He serves as president of the American Association of Neuropathologists and is on the editorial boards of more than 70 journals including the American Journal of Pathology and the Journal of Biological Chemistry. He also is co-editor-in-chief of the Journal of Alzheimer's Disease, the leading journal for Alzheimer research.
Source:
Christi Fish
University of Texas at San Antonio