The QC enzyme inhibitor reduces production of pyroglutamate Aβ, a particularly toxic, sticky form.
White blood cells from certain Parkinson’s patients react to α-synuclein peptides. Is this autoimmune reaction why the major histocompatibility complex is genetically linked to the disease?
The discovery hints that microglia, rather than neurons, may control much of a person’s genetic susceptibility to Alzheimer’s disease.
In a human cell model, VCP variants trigger a cascade of neuronal disruption and hobble astrocytes’ ability to support motoneurons.
Mutations in certain E. coli genes extend the lives of both normal and Aβ-laden roundworms.
Tomlinson was the first to quantify plaques and tangles in the postmortem brain, launching the modern era of Alzheimer’s research.
New diagnostic guidelines on dementia with Lewy bodies fold in science about sleep and the heart, two aspects that distinguish this disorder from Alzheimer’s and Parkinson’s.
Study of A673T carriers strengthens case for reducing Aβ to prevent AD.
In the past, researchers used to focus on the effect of Alzheimer’s disease risk genes in neurons. A new genetic study cements an ongoing shift of the spotlight toward microglia instead. It clarifies how a majority of AD genes are expressed primarily in these myeloid cells. Intriguingly, many of those genes are under the control of the master microglial transcriptional regulator, PU.1. The authors identified a genetic haplotype that lowered PU.1 expression and delayed AD onset in a large case-control study.
Casting a genome-wide net to snag E. coli mutants that affect longevity of their C. elegans hosts, researchers found 29 genes whose deletion lengthened the worms’ lifespan. Fourteen of them also kept amyloid-expressing worms alive longer. One of the apparent longevity-promoters is colanic acid, a polysaccharide that modulates the mitochondrial stress response.
After more than a decade, guidelines on how to diagnose and manage dementia with Lewy bodies have gotten a much-needed makeover. Leading clinicians now more clearly spell out clinical features and biomarkers that define this disease. They also added new insight about sleep and heart function that help distinguish DLB from Alzheimer’s and Parkinson’s. The reboot is timely, given that researchers will soon need to find patients for clinical trials dedicated to DLB.
Five years ago, Icelandic geneticists uncovered a mutation in the amyloid precursor protein (APP) that protected carriers against developing AD, ostensibly by decreasing production of Aβ peptides. Now, for the first time, researchers report a reduction in plasma Aβ by an average of 28 percent in carriers of this protective APP A673T mutation. The work provides more support for the amyloid-cascade hypothesis, and suggests that modestly reducing Aβ over a lifetime could provide a way to prevent AD.
- Terrence Town on Hot DAM: Specific Microglia Engulf Plaques
- Milos Ikonomovic on New Alzheimer’s Drug Shows Safety, Hints of Efficacy in Phase 2
- Cristina Muscio on DLB Guidelines Get a Makeover
- Satoru Funamoto on Substrate Says—APP Fragments Determine Where γ-Secretase Cuts
- Oleg Butovsky on Microglial Master Regulator Tunes AD Risk Gene Expression, Age of Onset
- Li-Huei Tsai and Elizabeth Gjoneska on Microglial Master Regulator Tunes AD Risk Gene Expression, Age of Onset
- Angel Golimstok on DLB Guidelines Get a Makeover
- Aditi Gurkar on Longevity Through Gut Bacteria? It Works in Worms
- Robert Moir on Longevity Through Gut Bacteria? It Works in Worms
- John Hardy on Microglial Master Regulator Tunes AD Risk Gene Expression, Age of Onset
- Roy Weller on “Father of AD Neuropathology” Sir Bernard Tomlinson dies at 96
- Michal Schwartz, Marco Colonna and Ido Amit on Hot DAM: Specific Microglia Engulf Plaques
- Samantha Burnham on At Risk, or Already Alzheimer’s? Elevated Aβ Predicts Cognitive Decline
- Henrik Zetterberg on At Risk, or Already Alzheimer’s? Elevated Aβ Predicts Cognitive Decline
- Stefan Lichtenthaler on More Support for Amyloid Hypothesis: Protective APP Mutation Lowers Aβ in Blood
- John Hardy on More Support for Amyloid Hypothesis: Protective APP Mutation Lowers Aβ in Blood
- Dennis Selkoe on Robert D. Terry, 93, Co-Founder of U.S. Alzheimer’s Research
- Harald Steiner on Substrate Says—APP Fragments Determine Where γ-Secretase Cuts
- Curt Freed on New Role for Parkinson’s Gene DJ-1: DNA and Protein Repair
- Tiago Outeiro on New Role for Parkinson’s Gene DJ-1: DNA and Protein Repair
- Mark Cookson on New Role for Parkinson’s Gene DJ-1: DNA and Protein Repair