Roughly one hundred years ago at a meeting of Bavarian psychiatrists, Dr. Alois Alzhiemer presented the intriguing case of his patient, Auguste D., a 51 year-old female admitted to the local asylum with presenile - mentia. He would argue that speci?c lesions in and around neurons were responsible for dementia. In the ensuing decades, studies of her disorder, which would be named Alzheimer’s disease (AD), were largely limited to descriptive neuropathological and psychological assessment of this disease with little understanding of the molecular and cellular mechanisms underlying neurodegeneration and dementia. This would change in the 1980’s when the protein components of the major neuropathological hallmarks of the disease, senile plaques (and cerebral blood vessel amyloid) and neuro?brillary tangles were ?rst determined. The identi?cation of the ?-amyloid protein (A?) and the microtubule-associated tau protein as the main components of plaques and tangles, respectively, would pave the way for the molecular genetic era of AD research. By the late-1980’s, the genes encoding the ?-amyloid precursor protein (APP) and tau (MAPT) were identi?ed and would subsequently be shown to harbor autosomal dominant mutations causing early-onset familial AD and frontal temporal dementia (FTD), respectively. Later, in the early 1990’s the ?4 variant of the apoliprotein E gene (APOE) would be found to be associated with increased risk for late-onset AD. Fundamental differences were soon noted between these two AD genes: APP and APOE.
There has been no scholarly research volume on Alzheimer’s Disease published in the last 3-5 yearsThe editors are leaders in the field and have assembled many other leading researchers as contributors