Problems during aging (Alzheimer's and others)

Abstract

Alzheimer's disease (AD) represents the most prevalent form of senile dementias. The disease is characterized by the occurrence of extracellular plaques, intracellular neurofibrillary tangles, a loss of neurons and synapses, hippocampus atrophy, and memory loss. Extracellular plaques consist mainly of beta-amyloid peptides (Abeta), which are generated through proteolytical cleavage of the larger amyloid precursor protein (APP). Mutations in the APP gene as well as in the presenilin genes (PS1/PS2) are responsible for the majority of familial AD (FAD) cases. All these mutations lead to an enhanced Abeta deposition in which mostly the generation of the longer Abeta variant containing 42 amino acids (Abeta42) is favored. In this chapter, the clinical features of AD, mild cognitive impairment being a transitional stage between the cognitive changes during normal aging and AD, as well as background in AD genetics, pathology, transgenic animal models, current and future therapy options, and risk factors such as diabetes and hypertension will be discussed.