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TORONTO and CAMBRIDGE, Mass., May 12, 2021 (GLOBE NEWSWIRE) ProMIS Neurosciences, Inc. (TSX: PMN); (OTCQB: ARFXF), a biotechnology company focused on the discovery and development of antibody therapeutics selectively targeting toxic oligomers implicated in the development of neurodegenerative diseases, today announced the appointment of Rudolph Tanzi, Ph.D, as Chair of the Company s scientific advisory board (SAB). Dr. Tanzi is the Joseph P. and Rose F. Kennedy Professor of Neurology at Harvard University and Vice-Chair of Neurology, Director of the Genetics and Aging Research Unit, and Co-Director of the Henry and Allison McCance Center for Brain Health at Massachusetts General Hospital.
William Bast Obituary (2021) - La Crosse, WI - La Crosse Tribune legacy.com - get the latest breaking news, showbiz & celebrity photos, sport news & rumours, viral videos and top stories from legacy.com Daily Mail and Mail on Sunday newspapers.
Some investigational Alzheimer’s disease therapies are more effective when paired with a treatment geared toward improving drainage of fluid and debris from the brain, according to a study in mice.
Experimental Alzheimer’s drugs have shown little success in slowing declines in memory and thinking, leaving scientists searching for explanations.
The new findings in the journal
Nature, however, suggest that the brain’s drainage system known as the meningeal lymphatics plays a pivotal but underappreciated role in neurodegenerative disease, and that repairing faulty drains could be a key to unlocking the potential of certain Alzheimer’s therapies.
“The lymphatic system is how the garbage is cleaned out of the brain. If it’s not working, everything gets gummed up.
While over 170 Alzheimer s mouse models have been in use since the 1990s, those models mimic early-onset AD, also known as familial AD, which accounts for less than 5 percent of total AD cases. Until recently, scientists introduced mutations found in familial risk human genes, such as the amyloid precursor protein and presenilin 1, into the mouse genome to generate the mouse models. The UCI team decided to take a new approach by developing a mouse model better positioned to analyze causes of late-onset AD. Also called sporadic AD, this new model encompasses the remaining 95 percent of cases. We believed models developed on the rare familial type might be a reason therapies have worked in the lab but haven t translated into clinical trial success, said Frank LaFerla, professor of neurobiology & behavior and the study s co-senior author; he is also dean of the UCI School of Biological Sciences and director of the UCI Alzheimer s Disease Research Center. We decided it was time t