The Alzheimer’s Association recently awarded Jose Abisambra, assistant professor at the University of Kentucky and researcher at the Sanders-Brown Center on Aging, a $100,000 New Investigator Research Grant to fund his work into understanding the function of a brain protein that alters during the development of Alzheimer’s disease. The association is the largest nonprofit supporter of research on Alzheimer’s, and these grants are meant to improve the understanding of the disease, as well as enhance the possibilities of finding a cure and advance the healthcare provided to patients.
“This grant is part of the Alzheimer’s Association’s effort to increase the number of scientists conducting Alzheimer’s research by supporting early-career development that will lay the groundwork for future research grant applications to the Alzheimer’s Association and other research funders,” explained executive director of the Alzheimer’s Association of Greater Kentucky and Southern Indiana, Teri Shirk, about the award, which can only be granted to investigators with a research career of less than ten years.
Abisambra has been studying the brain protein tau, which is responsible for the stabilization of microtubules. These tubular structures are the ones that contribute to cell structure maintenance. When tau registers abnormal modifications, it is an indication of cell death, which is dominant in the brains of patients suffering from Alzheimer’s. However, the researcher hasn’t been able to identify neither the causes for tau abnormalities, nor the reasons for the toxicity of the tau’s structures.
“A major challenge in the field of Alzheimer’s research is that we haven’t identified how tau causes neuronal damage and impairs memory,” the researcher said, as he explained that he had already found “compelling evidence,” as well as from other labs that indicate that “abnormal and toxic tau associates very strongly with ribosomes.” The ribosome is the hub of new protein production, and the process of memory formation is damaged when protein synthesis is reduced, he said.
“We were shocked to find that the abnormal association between tau and ribosomes potently reduced ribosomal function. Our research will lead to a better understanding of the process by which tau mediates ribosomal damage and how this phenomenon impairs memory in Alzheimer’s disease. This understanding is crucial to develop new therapeutic strategies, which are urgently needed,” Abisambra added.