Alzheimer disease (AD), a progressive neurodegenerative disorder, is the most common type of dementia, occurring in mid to late life. The neuropathological hallmarks of this disease include the presence of extracellular deposits of highly fibrillogenic Aβ42 peptides in senile plaques and intraneuronal accumulations of hyperphosphorylated τ in neurofibrillary tangles (see Giulian 1999 [in this issue]). Although most cases of AD occur as age-associated disorders, autosomal dominant inheritance of mutant genes encoding the β-amyloid precursor protein (APP), presenilin 1 (PS1), or presenilin 2 (PS2) cause early-onset AD in several families (i.e., familial AD [FAD]; for review, see Price and Sisodia 1998).