ABSTRACT
Neither β-amyloidosis nor neurofibrillary degeneration is unique to AD, but disorders with the latter lesion called tauopathies (e.g. FTDP17, dementia pugilistica, Pick disease, corticobasal degeneration) are associated with dementia. The neurofibrillary degeneration of the Alzheimer type is seen only sparsely in aged animals and in experimentally induced conditions. Thus, all these findings taken together suggest that neurofibrillary degeneration plays a pivotal role in the pathogenesis of AD and related tauopathies and that inhibition of this lesion is a promising therapeutic target for these diseases. Identification of specific therapeutic pharmacological targets requires understanding of the molecular mechanism by which this lesion might cause neurodegeneration.
