Women May Keep Verbal Memory Skills Longer than Men in the Early Stages of Alzheimer’s

Newswise, March 18, 2016 – Women may have a better memory for words than men despite evidence of similar levels of shrinkage in areas of the brain that show the earliest signs of Alzheimer’s disease, according to a study published in the March 16, 2016, online issue of Neurology®, the medical journal of the American Academy of Neurology

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According to study author Erin E. Sundermann, PhD, of Albert Einstein College of Medicine in Bronx, NY, “One way to interpret the results is that because women have better verbal memory skills than men throughout life, women have a buffer of protection against loss of verbal memory before the effects of Alzheimer’s disease kick in.

Because verbal memory tests are used to diagnose people with Alzheimer’s disease and its precursor, mild cognitive impairment, these tests may fail to detect mild cognitive impairment and Alzheimer’s disease in women until they are further along in the disease.”

The study included participants from the Alzheimer’s Disease Neuroimaging Initiative: 235 people with Alzheimer’s disease, 694 people with mild cognitive impairment that included memory problems, and 379 people with no memory or thinking problems. The groups’ performance on a test of verbal memory was compared to the size of the hippocampal area of the brain, which is responsible for verbal memory and affected in the early stages of Alzheimer’s disease.

Women performed better than men on the tests of both immediate recall and delayed recall among those showing evidence of minimal to moderate amounts of hippocampal shrinkage.

At the high level of hippocampal shrinkage, there was no difference in the scores of men and women. At the score that indicates the start of verbal memory impairment, or 37 on a scale of zero to 75 for immediate recall, women showed greater evidence of hippocampal shrinkage (ratio of hippocampal volume to total brain volume multiplied by 103 was 5 compared to 6 for men).

Mary Sano, PhD, of Icahn School of Medicine at Mount Sinai in New York, NY, and a member of the American Academy of Neurology, said in a corresponding editorial, “At a public policy level, the potential health care cost for under-detection or delayed diagnosis of women with Alzheimer’s disease or its early stages is staggering and should motivate funding in this area.”

“If these results are confirmed, then we may need to adjust memory tests to account for the difference between men and women in order to improve our accuracy in diagnosis,” said Sundermann.

The Alzheimer’s Disease Neuroimaging Initiative was supported by the National Institute on Aging, National Institute of Biomedical Imaging and Bioengineering, Alzheimer’s Association, Alzheimer’s Drug Discovery Foundation, U.S. Food and Drug Administration, Abbott, Amorfix Life Sciences, AstraZeneca, Bayer HealthCare, BioClinica, Biogen Idec, Bristol-Myers Squibb, Eisai, Elan Pharmaceuticals, Eli Lilly, F. Hoffmann-La Roche and Genentech, GE Healthcare, Innogenetics, IXICO, Janssen Alzheimer Immunotherapy Research and Development, Johnson and Johnson Pharmaceutical Research and Development, Medpace, Merck, Meso Scale Diagnostics, Novartis Pharmaceuticals; Pfizer, Servier, Synarc and Takeda Pharmaceutical.

To learn more about Alzheimer’s disease, please visit www.aan.com/patients.

The American Academy of Neurology, an association of 30,000 neurologists and neuroscience professionals, is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Alzheimer’s disease, stroke, migraine, multiple sclerosis, brain injury, Parkinson’s disease and epilepsy.

Researchers Find Some Evidence of Link Between Stress, Alzheimer’s Disease

Newswise, September 21, 2015 — University of Florida Health researchers have uncovered more evidence of a link between the brain’s stress response and a protein related to Alzheimer’s disease.

The research, conducted on a mouse model and in human cells, found that a stress-coping hormone released by the brain boosts the production of protein fragments. Those protein pieces, known as amyloid beta, clump together and trigger the brain degeneration that leads to Alzheimer’s disease.

The findings were published recently in The EMBO Journalby a group that includes Todd Golde, M.D., Ph.D., director of the UF Center for Translational Research in Neurodegenerative Disease and a professor in the UF College of Medicine’s department of neuroscience.

The research contributes to further understanding the potential relationship between stress and Alzheimer’s disease, a disorder believed to stem from a mix of genetic, lifestyle and environmental factors.

The findings strengthen the idea of a link between stress and Alzheimer’s disease, Golde said.

“It adds detailed insight into the stress mechanisms that might promote at least one of the Alzheimer’s pathologies,” Golde said.

Figuring out the non-genetic factors that heighten the risk of Alzheimer’s disease is especially challenging, and the recent study is one step in a long process of looking at the effects of stress and other environmental factors, according to Golde. It could also point the way to a novel treatment approach in the future, he said.

Here is what researchers found: Stress causes the release of a hormone called corticotrophin releasing factor, or CRF, in the brain.

That, in turn, increases production of amyloid beta. As amyloid beta collects in the brain, it initiates a complex degenerative cascade that leads to Alzheimer’s disease.

During laboratory testing, mouse models that were exposed to acute stress had more of the Alzheimer’s-related protein in their brains than those in a control group, researchers found.

The stressed mice also had more of a specific form of amyloid beta, one that has a particularly pernicious role in the development of Alzheimer’s disease.

To better understand how CRF increases the amount of Alzheimer’s-related proteins, researchers then treated human neurons with CRF.

That caused a significant increase in the amyloid proteins involved in Alzheimer’s disease.

Those and other complex experiments reveal more about the mechanics of a likely relationship between stress and Alzheimer’s disease.

The stress hormone, CRF, causes an enzyme known as gamma secretase to increase its activity. That, in turn, causes more of the Alzheimer’s-related protein to be produced, Golde said.

Modifying environmental factors such as stress is yet another approach to warding off Alzheimer’s disease, and one that is easier than modifying the genes that cause the disorder, Golde said. One possible solution — blocking the CRF receptor that initiates the stress-induced process that generates Alzheimer’s-related proteins — didn’t work. Researchers are now looking at an antibody that could be used to block the stress hormone directly, Golde said.

“These softer, non-genetic factors that may confer risk of Alzheimer’s disease are much harder to address,” Golde said. “But we need more novel approaches in the pipeline than we have now.”

The idea of looking more closely at the mechanism linking stress and Alzheimer’s disease came from Seong-Hun Kim, M.D., Ph.D., a former assistant professor in the College of Medicine’s department of pharmacology and therapeutics and now a psychiatrist in Seattle.

Much of the project’s experiments were done by Hyo-Jin Park, Ph.D., who was a postdoctoral associate during the project and is now an assistant scientist in the College of Medicine’s department of aging and geriatric research. Kevin Felsenstein, Ph.D., an associate professor of neuroscience in UF’s College of Medicine, also made major contributions to the work.

The research was supported by multiple grants from the National Institutes of Health and the U.S. Department of Veterans Affairs.