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Posts tagged as “AD”

‘Young Blood’ Researchers Are Still in the Pursuit to Stall Aging, Slow Alzheimer’s | Being Patient


"Earlier this year, the F.D.A. issued a warning to Ambrosia, a company that was selling plasma transfusions of 'young blood' to elderly people, suggesting it may stop aging. While the F.D.A. announced there is 'no proven clinical benefit' of these transfusions, it’s not the first time the practice has been pursued: Stanford researchers published a study on young blood transfusions 2017."a @href="https://www.beingpatient.com/alkahest-young-blood-chronokines/"> Read the full story at beingpatient.com

More evidence that blood tests can detect the risk of Alzheimer’s | Eureka Alert

"A new study confirms that a simple blood test can reveal whether there is accelerating nerve cell damage in the brain. The researchers analysed neurofilament light protein (NFL) in blood samples from patients with Alzheimer's disease. Recently published in JAMA Neurology, the study suggests that the NFL concentration in the blood could be able to indicate if a drug actually affects the loss of nerve cells."

Parsing How Alzheimer’s Genetic Risk Works Through Microglia | Alz Forum

"Much of the genetic risk of Alzheimer’s disease plays out in microglia. But exactly how do risk variants change these cells? At the 14th International Conference on Alzheimer’s and Parkinson’s Diseases, held March 27–31 in Lisbon, Portugal, speakers filled in some gaps, and discussion of this question buzzed in the hallways all week. Christian Haass of the German Center for Neurodegenerative Diseases in Munich characterized progranulin as TREM2’s opposite. While mutations in TREM2 suppress microglial activation, mutations in progranulin permanently rev them up into voracious, toxin-spewing machines. Other speakers associated GWAS hits in general, and the MS4A gene cluster in particular, with hyperactive, damaging microglia. Researchers also highlighted potential therapeutic targets among microglial genes. Two talks presented evidence that suppressing the CD33 receptor can contain amyloidosis (see Part 5 in this series), while another fingered BIN1 as a key culprit in propagating phosphorylated tau."