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Auriel Willette, an ISU assistant professor of food science and human nutrition who led the study, says the researcher who initially discovered the gene, TOMM40 (Translocase of Outer Mitochondrial Membrane-40kD), found it increased the risk for Alzheimer's. However, when multiple studies failed to replicate the results, many researchers dismissed the findings, Willette said. Not convinced the gene was a total bust, Willette decided to look at other factors that may be contributing to the mixed results. In the paper published online by  Alzheimer's & Dementia : The Journal of the Alzheimer's Association as an in press corrected proof, Willette and his colleagues found a dramatic difference in the gene's impact on memory, general cognitive function and risk based on a family history of Alzheimer's disease and the length of a specific section of the gene. "It was kind of a shot in the dark, but we found if you don't have a family history of Alzheimer...

The finding potentially could explain the mechanism by which Alzheimer's, Parkinson's, Huntington's, and other neurodegenerative diseases spread within the brain and disrupt normal brain functions. The finding also suggests that an effective treatment  for one neurodegenerative disease might work for other neurodegenerative diseases as well. The study by senior author Edward Campbell, PhD, first author William Flavin, PhD, and colleagues is published in the journal  Acta Neuropathologica . "A possible therapy would involve boosting a brain cell's ability to degrade a clump of proteins and damaged vesicles," Campbell said. "If we could do this in one disease, it's a good bet the therapy would be effective in the other two diseases." Neurodegenerative diseases are caused by the death of neurons and other cells in the brain, with different diseases affecting different regions of the brain. Alzheimer's destroys memory, while Parkinson...

The findings, which appear in the journal  eLife , may one day lead to better therapies and treatments for these diseases. The prion protein plays a crucial role in fatal neurodegenerative  disorders like Creutzfeldt-Jakob disease in humans and "mad cow disease" in cattle. Prion diseases are part of larger group of human neurodegenerative disorders, including Alzheimer's, Parkinson's and Huntington's diseases, which are all due to the abnormal accumulation of protein aggregates in the brain. According to the researchers, how nerve cells are damaged in these diseases has remained a mystery until now. "Our work shows that the prion protein acts like a molecular on-off switch. In the "on" positon, one end of the protein delivers a toxic signal to nerve cells, while in the "off" position, the other end of the protein serves as a brake to reduce the toxic signal. Moreover, copper, a metal that is a normal component of brain biochemistry, ...

Every day billions of people across the planet successfully navigate their environments, for example when they go to work or head home. Such journeys generally happen with little conscious effort and rest on the brain's ability to use overall knowledge of an environment to make estimates of where it finds itself. The ability to make fine grained assessments of location is seated in the hippocampus, a seahorse-shaped structure located in the temporal lobe. Research shows that the precise mechanism for navigation includes hippocampal place cells, which increase or decrease in electrical activity depending on one's location. However, when making their daily commute, people don't need very detailed representations of which houses they pass in which order. Instead, they can make due with more course information. Left at the museum and somewhere down the road right again at the supermarket, called topographical orientation. Building on current research, the researchers invest...