By Cleaving GABA(A) Receptors, BACE1 Lifts Lid on Hyperactivity
In a mouse model of amyloidosis, the BACE1 enzyme snipped subunits of the GABA(A) receptor, squelching its inhibitory function.
NEWS
Do Specialized Glycoproteins Prop Up Blood-Brain Barrier?
Thinning out glycoproteins in the brain blood vessels of young mice allowed blood to leak into the brain. Promoting glycosylation in old mice strengthened the barrier.
Parkinson’s Risk Gene Speeds Spread of α-Synuclein Pathology
In neurons, FAM171A2 opens the door to toxic fibrils. An approved cancer drug slams it shut.
Hot News: DIAN Participant Defies Presenilin 2 Mutation
The man has lots of plaques but few tangles 18 years after his expected age of onset; potential protective factors include extensive heat shock protein expression.
Could Taking Down a DNA Repair Protein Stave Off Huntington’s?
In neurons from a person with HD, knocking down MSH3 kept CAG nucleotide expansions from growing even longer.
Plasma p-Tau217 Flags Alzheimer’s Pathology in Other Disorders
The marker detected plaques and tangles with 90 percent accuracy in almost 200 autopsy-confirmed frontotemporal dementia cases.
Does COVID-19 Push People Toward Alzheimer’s? New Data Say Yes.
Plasma Aβ42/40 ratios drop in people soon after COVID-19 infection even for mild cases. Does this mean they are at higher risk for dementia?
Studying Diverse Populations May Require New Biomarkers
Amyloid and tau accumulation patterns differ in black, white, and Hispanic people.
SPOTLIGHT
Do Specialized Glycoproteins Prop Up Blood-Brain Barrier?
It appears that bristly, bottlebrush-shaped glycoproteins on the interior of brain blood vessels control their permeability. These glycoproteins dwindle with age. Restoring them in old mice firmed up the barrier, while removing them in young mice caused vessels to leak blood. The glycoproteins wane in Alzheimer’s and Huntington’s diseases.
Hot News: DIAN Participant Defies Presenilin 2 Mutation
Boasting resilience to amyloid, Doug Whitney, a DIAN participant with the Volga PS2 mutation, has many plaques but few tangles, and he remains cognitively healthy 18 years past the age when Alzheimer's symptoms were estimated to start. Multiomic analyses suggest protective variants in CD33, tau, and other genes, but also an intriguing abundance of heat shock proteins and of metabolic factors implicated in aging research.
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