Right sizing funding for Alzheimer's disease

Perhaps the most striking example of recent success in curbing a major emerging epidemic is HIV/AIDS. Within two decades of the identification of HIV as the cause of AIDS, rapid development of multiple anti-viral therapies turned a rapidly progressive and fatal disease into a more chronic disease, at least in industrialized nations [3,4]. Of course, there are no widely deployable cures yet for HIV/AIDs, and it is still a potentially lethal disease. Moreover, anti-viral pharmacotherapy needed to control disease progression has numerous and significant side effects. Nevertheless, given the continued progress, there is reasonable hope that either prophylaxis with vaccines or further advances in anti-viral therapies will further reduce or eliminate HIV-related morbidity and mortality. Notably, the historical timelines for discovery of the presumed causative agents of HIV and AD are similar, with HIV definitively identified in 1981 and the suspected protein triggers of AD identified in the mid-1980s, with strong links to causality established for amyloid beta (Aβ) and tau aggregates established in the 1990s.Given this interesting parallel in timelines for HIV/AIDs and AD, it is worthwhile to explore the question: "Why have we not made more inroads with respect to disease-modifying therapeutics for AD?" This question needs to be asked in the context of the question: "What factors were enabling in the development of novel anti-HIV therapies?" Although there are certainly many germane medical and scientific issues, one critical aspect may simply be that the funding for HIV/AIDs research, at least in the United States, appears to have been sufficient, and therefore in retrospect "right sized", to enable not only basic understanding of the disease-causing entity and the disease it causes but also to translate that enhanced understanding into novel and effective therapeutics.If one assumes that funding for HIV/AIDS was right sized to enable translation of basic discoveries to