Alzheimer's disease, the most common form of senile dementia, affects more than 15 million people world-wide and is characterized by a marked deterioration in memory and all cognitive functions, as a result of a progressive degeneration and loss of cortical and limbic neurons. This process is associated with the presence of both the so-called -amyloid deposits and the cellular neurofibrillary tangles composed mainly of paired helical filaments of aberrantly hyperphosphorylated tau protein. The accumulation of ubiquitin in neurofibrillary tangles and senile plaques (both characteristic of the neuronal abnormalities associated with the disease) is postulated to play a role in the repair mechanism related to neuronal regeneration.

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