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Under the microscope: SBU professors analyze link between amino acid and Alzheimer’s disease

Dr. William Van Nostrand is one of two professors working on experiments that use mice to test relative cognitive decline. (JESSICA DESAMERO / THE STATESMAN)
Dr. William Van Nostrand is one of two professors working on experiments that use mice to test relative cognitive decline. (JESSICA DESAMERO / THE STATESMAN)

Every other week, Ruchi Shah, a sophomore biology major, will take a look at Stony Brook-related research and science news.

Amyloid β is known to play a role in Alzheimer’s disease, but recent findings by Dr. William Van Nostrand, professor of neurosurgery, and Dr. John Robinson, professor of psychology at Stony Brook University, and their teams defined a model of the link between the location of Amyloid β deposits and cognitive decline.

Amyloid β accumulation in the brain leads to plaques, which can promote cognitive decline associated with Alzheimer’s disease. Van Nostrand and Robinson aimed to further understand the disease by studying the role that the location of amyloid deposition in the brain plays.

Amyloid β can accumulate around neurons and around blood vessels in the brain. To compare the relative impact that Amyloid β accumulation has in the two locations, Van Nostrand and Robinson used two mouse models, which develop amyloid deposits at the same rate. The only difference between the two strains is that one develops plaques around the neurons, while the other strain develops plaques around the blood vessels.

A Barnes Test was used to test the relative cognitive decline of the two strains of mice as the amyloid deposits developed. In this test, the mice are put into a bright, raised platform with eight equidistant holes. There are reference points around the holes, differentiating each of them. Only one of the holes is an escape hole through which the mouse can return to its preferred, dark environment. All of the mice were given time to explore the chamber and become accustomed to finding the escape hole. After the training period, when normal mice are put back into the chamber, they are able to quickly remember where the escape hole was.

As the two mouse strains began to develop their amyloid deposits, those with the accumulation around the blood vessels took longer to find the escape hole than those with accumulation around neurons. Van Nostrand explained that while Amyloid β accumulation in both locations will eventually cause impairment, as “the vascular component is an earlier driver of cognitive decline.”

Using imaging and staining systems, Van Nostrand and his team were able to quantify the amount of Amyloid β and found that there was a higher quantity of the protein in the plaques around the neurons, even though these plaques did not have as much of an impact on cognitive decline.

Overall, this study shows that blood vessel deposits affect cognitive decline differently than plaques around neurons, and the research team now aims to understand the basis of that difference. They plan to investigate structural differences between the two types of amyloid deposits as well as differences in the responses the two deposits activate. For example, some plaques are known to activate types of inflammatory cells called microglia. In previous studies, they have found that suppressing the microglia cells by using anti-inflammatory drugs results in a cognitive improvement. Therefore, the results of this study are important because the plaques around the blood vessels can be targeted in the future as a therapy for Alzheimer’s disease.

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