Tags

, , ,

By Heather Wilkins

Heather Wilkins-finalWe all have Alzheimer disease (AD) on our brain, no pun intended. With daunting projections indicating the number of people afflicted with AD will triple within the next few decades, it’s not an issue we can afford to ignore. AD received some much needed media attention following the Alzheimer’s Association International Conference in July 2015, and this exciting momentum has since continued.

The most promising development in the AD research field is the much needed increase in funding from the National Institutes of Health (NIH). The overall goal of this funding boost is to find viable treatments and/or prevention plans by 2025 (PDF). The current proposal calls for an additional $323 million in research funding.

Beyond a significant increase in AD research funding, the media has focused on publicizing cutting edge scientific developments. These include early clinical trial findings, potential blood based biomarker risk assessment methods, and new hypotheses regarding the underlying cause of AD. However, what is daunting regarding AD research is we still do not fully understand some of the basic mechanisms of this disease.

Since Alois Alzheimer described his experience with the first recognized AD patient in 1906, scientists have known that two proteins within the brain, tau and amyloid beta, form insoluble tangles and aggregates, respectively. These aggregates and tangles are toxic to the brain. These findings formed the basis for the two main hypotheses for Alzheimer etiology: the amyloid cascade hypothesis and the tau hypothesis. These hypotheses state that either amyloid beta or tau are the causative factor leading to AD pathology. The majority of disease models are based on these two hypotheses.

Other findings, such as reduced brain glucose metabolism, increased AD risk if your mother is afflicted, and association of AD with type 2 diabetes (PDF), have led to the development of alternative hypotheses. In particular, these findings bring to light a strong relationship between pathological hallmarks of AD and mitochondrial function. Mitochondria are the powerhouses of cells; working to produce energy, modulate cell signaling, and numerous other critical cell processes. The mitochondrial cascade hypothesis, developed by Russell Swerdlow, states mitochondrial function is the causative factor leading to AD pathology, including amyloid plaques and tau tangles.

These “alternative” hypotheses have begun to receive more funding. Yet, there is still great need for expanded research opportunities and ideas. As Seth Rogen commented during his statement to the U.S. Senate in 2014, young scientists are opting to pursue other career avenues due to lack of funding and job opportunities, as well as the uncertainty of future prospects. Rogen and his wife, Lauren Miller, founded Hilarity For Charity, where they raise funds that are donated to benefit AD research, care, support, and awareness. There are several national private foundations that support AD research including (but not limited to) the Bright Focus Foundation, Alzheimer’s Drug Discovery Foundation, and the Alzheimer’s Association. There are also regional organizations that support local cutting edge AD research studies.

The future of AD research needs to encompass integrated and collaborative efforts, especially among scientists with new testable hypotheses. Even more important, AD research requires young activists and scientists. Unfortunately, all of these efforts require significant financial support to succeed. Without this, we will not be able to reach the 2025 goals set forth by the national plan.

Heather Wilkins, Ph.D., is a postdoctoral fellow at the University of Kansas Medical Center in the Department of Neurology and the University of Kansas Alzheimer Disease Center.