Introduction: The molecular pathogenesis of Alzheimer's disease (AD) includes a variety of risk factors, extracellular deposition of β-amyloid, accumulation of intracellular neurofibrillary tangles, oxidative neuronal damage and inflammatory cascades. Although amyloid-β-containing senile plaques and phospho-tau-containing neurofibrillary tangles are hallmark lesions of AD, neither is specific to nor even a marker of the disease. From a biochemical point of view the most consistent finding is a decreased level of choline acetyltransferase. In recent years, cumulative evidence has been gained on the involvement of neuronal lipoprotein activity, and on the role of cholesterol and other lipids in pathogenesis. Although basic research has made remarkable progress in the past two decades, currently available drugs are only able to improve cognitive symptoms temporarily and no treatment can reverse, stop or even slow this inexorable neurodegenerative process.
Areas covered: The various neurobiological events associated with development of AD and the multiple treatment approaches for combating this disorder.
Expert opinion: AD is a complex multifactorial disorder and thus a single target or pathogenic pathway is unlikely to be identified. Developing therapeutic interventions demands a greater understanding of the processes and the differential involvement of the various mediators. Effective therapeutics are urgently needed, and it is hoped that anti-amyloid strategies will offer a significant step towards a causal therapy.