Why delay in effective treatment for Alzheimer's disease and related conditions

Alzheimer's disease (AD) was first described by Alois Alzheimer in 1906 but the protein composition of neurofibrillary tangles and amyloid plaques was not decoded till about seven to eight decades later, respectively. The bulk of studies during the last four decades were focused on Aβ amyloid and led to many human clinical trials, none of which showed any beneficial therapeutic effects. Though the outcome of prodromal Aβ immunotherapy in carriers of AD-causing gene mutations is still awaited, this has led to a shift away from Aβ-based, toward tau-based, therapeutic approaches. Currently, several Phase I and Phase II human clinical trials are underway, the majority of which involve active or passive tau immunization. It is quite possible that along with inhibition of tau pathology, use of neurotrophic compounds that can enhance neurogenesis and neuronal plasticity will be required to effectively prevent and restore cognitive deficits in AD and related conditions. Investments need to be made in drug development of such compounds.