Glial cells and aβ peptides in alzheimer's disease pathogenesis

Alzheimer's disease (AD) is a tragic neurodegenerative disorder that targets the elderly and ultimately ends in dementia. Unfortunately, the ever increasing length of the human life span in the United States and throughout the world is now being paralleled by corresponding increases in the incidence of AD as well as in the duration of this disease in individual patients. AD is characterized symptomatically by progressive cognitive and memory loss, language deficits, impairment of judgment, deficient problem solving, and reduced abstract thought. At the root of these symptoms is widespread loss of neurons and their synapses primarily in the cerebral cortex, entorhinal area, hippocampus, ventral striatum, and basal forebrain [1]-[5]. Other pathological features that make their appearance in the brain tissue include a variety of different kinds of amyloid deposits collectively called amyloid plaques (Fig. 13.1), persistent accumulations of abnormal tau filaments referred to as neurofibrillary tangles, dense focal deposits of fibrillar amyloid in the walls of certain blood vessels (mostly small arterioles), intraneuronal accumulation of amyloid, reactive gliosis, and inflammation [1], [2], [6]-[9].