Mice lacking the receptor have more diffuse plaques, more dystrophic axons, and more neurodegeneration. The TREM2-microglia hail from inside the brain.
In mammalian cells, worms, and mice, Aβ snags yeast and bacteria in a fibril mesh, preventing their assault on host cells.
Age-related attrition of the male chromosome in blood cells raises the risk of Alzheimer’s disease. Researchers suspect immune cells are compromised.
A compound that binds mGluR5, a potential Aβ receptor, lowered amyloid pathology and improved cognition in two mouse models of Alzheimer’s disease.
A small trial suggests the drug liraglutide bolsters glucose metabolism in the brains of people with Alzheimer’s, but whether this modifies their disease remains unknown.
Researchers find high levels of certain pesticides in the blood of people with ALS, while in neuronal cultures some of them caused gene expression changes reminiscent of Alzheimer’s.
Nuances in episodic memory can tell if primary progressive aphasia is due to non-tangle types of tau pathology or to plaques and tangles.
Scientists match up PET scans of neurofibrillary tangles against Aβ imaging, CSF measures, and cognitive tests to see how biomarkers change relative to function.
Instead of gobbling up amyloid, microglia may instead pack it up so it does less harm to the brain. Support for this hypothesis comes from super-resolution microscopy. Researchers examined amyloid fibrils and surrounding cellular processes in exquisite detail, finding that TREM2-positive microglia erect a cellular barrier that compresses plaques and contains their toxicity. TREM2-deficient cells from people and from mice make weaker barriers, leading to more diffuse plaques, more dystrophic dendrites, and more neurodegeneraion. The microglia doing this come from inside the brain, another study finds.
For all the hubbub surrounding Aβ, researchers have yet to nail down a physiological function, if it has one. New evidence supports the idea that this tiny peptide plays a role in the innate immune system, waging cellular war on invading microbes. Its ability to oligomerize and fibrillize—the very properties shown to make it toxic to neurons—also enable it to form sticky lattices that trap yeast and bacteria. If independently confirmed, the findings could bolster the pathogen hypothesis of Alzheimer’s disease.
Man-made chemicals pervade our modern environment and many of them have been implicated as risk factors for neurodegenerative disease. Researchers used blood samples, and gene-expression profiling in neuronal cultures, to pinpoint potentially harmful compounds. They turned up evidence that older pesticides, and a new class of fungicides, may predispose some people to ALS, autism, and Alzheimer’s.
Researchers have tied sleep to clearance of waste products such as excess Aβ. New research suggests this clearance may be driven by a change in the extracellular ion composition, which swells the interstitial fluid. Intriguingly, a change in the ion balance alone can transition brains from wake to sleep states and vice versa. Other recent studies on Virchow-Robin spaces strengthen links between poor sleep, disrupted fluid flow, and neurological disease.
- Alcino Silva on In mTORC and Theta Rhythms, New Clues to How Sleep Locks Down Memories
- Jason Richardson on Pesticides Raise Risk of ALS and Potentially Alzheimer’s Disease
- Thomas Foltynie on Diabetes Drug May Rev Up Brain Metabolism in People with Alzheimer’s
- William Goure, Kalpana Merchant and Grant Krafft on Aβ Oligomers Purified from Human Brain
- Samuel Lockhart on On Multiple Marker Analysis, Tangles Track Best With Functional Decline
- Gil Rabinovici on On Multiple Marker Analysis, Tangles Track Best With Functional Decline
- Laure Saint-Aubert on On Multiple Marker Analysis, Tangles Track Best With Functional Decline
- Roxana Carare and Roy Weller on Sleep and Brain Cleansing—Fresh Insights into Regulation and Disruption
- Berislav Zlokovic on Sleep and Brain Cleansing—Fresh Insights into Regulation and Disruption
- Torik Ayoubi on Pathogenic Presenilin Mutations Generate Aβ43
- Tara Spires-Jones on Stress Granule Protein Entwines and Misfolds Tau