Incorporating genetic diversity into a mouse model of Alzheimer's disease resulted in greater overlap with the genetic, molecular and clinical features of this pervasive human disease, according to a study funded by the National Institute on Aging (NIA), part of the National Institutes of Health. The study also suggests that adding genetic diversity may be key to improving the predictive power of studies using mouse models and increasing their usability for precision medicine research for Alzheimer's. This research comes out of the newly established Resilience-Alzheimer's Disease Consortium (Resilience-AD) and was published online Dec. 27, 2018 in the journal Neuron.
"This is the first study to show that you can replicate many of the molecular features of Alzheimer's disease in a genetically diverse mouse model," said NIA Director Richard J. Hodes, M.D. "It points to a strategy for better use of mouse models for precision medicine research -- both basic and translational -- for Alzheimer's disease."
Alzheimer's disease is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills and, eventually, the ability to carry out simple tasks. As many as 5.5 million Americans age 65 and older are estimated to be living with Alzheimer's disease, the most common form of dementia.
(Score: 1, Interesting) by Anonymous Coward on Sunday December 30 2018, @02:30PM (1 child)
Unless a cell is functioning properly, you get amyloids. Thats why they are elevated in every single disease state ever checked. They are detected in like 60% of people with clinical akzhiemers, and 40% of elderly brains of people without symptoms of dementia.
There is zero reason to think amyloid-beta is a cause rather than a symptom. This is more waste of time/money research.
(Score: 1, Interesting) by Anonymous Coward on Monday December 31 2018, @03:32AM
Wrong.
Do you have some hidden evidence that disproves or a better explanation for why:
Populations with genetic determinants that specifically predispose them to producing amyloid beta in the brain develop early onset Alzheimer's at a much higher rate than non-carriers.
Populations with genetic determinants that predispose them to have inefficient clearance of amyloid beta in the brain have increased Alzheimer's risk than non-carriers.
"One proof is really quite simple - give the amyloid gene of different lengths (up to 42) to mice, and they develop symptoms in 10 months which mice normally don't (10 months is ancient for a mouse).
Trisomy 21(Downs) carriers in humans get Alzheimers very quickly (before 40), as the ABgene is on chr 21 a bad dosage gets amplified."
https://soylentnews.org/comments.pl?noupdate=1&sid=18030&commentsort=0&mode=threadtos&threshold=0&highlightthresh=0&page=1&cid=467758#commentwrap [soylentnews.org]
Also, other aggregation-prone protiens have been show to directly cause diseases in the brain and other organs.