Fully automated immunoassay could offer cost-effective screening for AD.
A meta-analysis of 47 studies suggests CSF NfL is particularly elevated in a select few, suggesting it could help in differential diagnosis.
In response to the peptide, these little cells squeeze capillaries, constricting them. This may contribute to neuronal dysfunction.
New strains have amyloid, neurodegeneration, and neuroinflammation, all against a background of natural genetic variation.
In healthy, older adults specific EEG patterns correlated with plaque and tangle burdens.
Using different techniques, contestants vied for the best way to tell which ADNI participants would develop clinical, cognitive, or imaging signs of Alzheimer’s disease.
Aβ deposits make distal neurons vulnerable to insults, including from local Aβ, says imaging study. The combination hastens cognitive decline.
One rare variant protects ApoE4 carriers, others put noncarriers at risk.
Virtual Exhibit Hall
Alzforum encourages users to visit the Virtual Exhibit Hall, where companies showcase their newest initiatives, products, and services. We welcome Dash Genomics, Inc. and Abcam, which join our other exhibitors — Biogen, BioLegend, BrainXell, NanoString Technologies, and the Jackson Laboratory.
Though amyloid plaques are a hallmark of Alzheimer’s disease, their distribution has never correlated well with cognitive decline. Now, scientists think they know why. According to new research, plaques weaken distant, connected neurons, making them vulnerable to stress. Nearby plaques then disrupt those vulnerable neurons, causing learning and memory problems. The study suggests that global and local Aβ conspire to bring about dementia.
In mice, myelin repair seems efficient only when pro-inflammatory microglia perish and pro-regenerative ones take their place. The old cells die by necroptosis, a type of programmed cell death. Microglial necroptosis and regeneration occur at sites of myelin repair in multiple sclerosis models. It remains to be see whether a similar cellular switcheroo happens in people or in other diseases that cause demyelination, including Alzheimer’s.
- Hugo Vanderstichele and Eugeen Vanmechelen on Drawing Closer: Alzheimer’s Blood Test for Primary Care
- Alberto Lleo on NfL: Useful in Differential Diagnosis?
- Costantino Iadecola on Aβ Acts Through Pericytes to Throttle Brain Blood Flow
- Marco Colonna and Simone Brioschi on Wild Mice Inject Genetic Diversity into Models of Alzheimer’s Disease
- Joanna Jankowsky on Wild Mice Inject Genetic Diversity into Models of Alzheimer’s Disease
- Barbara Bendlin on Do Brain Waves During Sleep Reflect Aβ and Tau Pathologies?
- Bernard Hanseeuw on Parsing Local and Distal Aβ Shows Links to Metabolism, Cognition
- David Jones on Parsing Local and Distal Aβ Shows Links to Metabolism, Cognition
- Marcus Raichle on Parsing Local and Distal Aβ Shows Links to Metabolism, Cognition
- Constanze Depp and Stefan Berghoff on Dead Microglia Pave the Way for Myelin Regeneration
- Greg Czyryca on Keep Your Enthusiasm? Scientists Process Brutal Trial Data
- Eva Czirr on Two Proteins in Young Blood Give Synapses a SPARC
- James Wallace on Serial PET Nails It: Preclinical AD Means Amyloid, Tau, then Cognitive Decline
- Oskar Hansson on Serial PET Nails It: Preclinical AD Means Amyloid, Tau, then Cognitive Decline
- Samuel Lockhart on Serial PET Nails It: Preclinical AD Means Amyloid, Tau, then Cognitive Decline
- Mark Cookson on Ubiquitin Ligase SCarFs Up Internalized α-Synuclein, Prevents Seeding
- Ruth Itzhaki on When Host Proteins Coat Virus, Amyloid Fibrils Form
- Doo Yeon Kim and Rudy Tanzi on Reproducible Brain Organoids Could Offer New Models for Research
- Stefan Lichtenthaler on NRF2/ARE pathway negatively regulates BACE1 expression and ameliorates cognitive deficits in mouse Alzheimer's models.
- Kariem Ezzat on When Host Proteins Coat Virus, Amyloid Fibrils Form
- Todd E. Golde and David R. Borchelt on When Host Proteins Coat Virus, Amyloid Fibrils Form