Survey of Tau Partners Highlights Synaptic, Mitochondrial Roles
An unbiased “interactome” generated from human neurons could shed light on what goes wrong in tauopathies, and help identify new therapeutic targets.
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Neuron-Specific Retromer Identified—Does It Stave Off Alzheimer’s?
When this retromer faltered in mice, Aβ levels rose in the brain and synaptic signaling waned in the transentorhinal cortex. General retromer loss in hippocampal neurons evoked dystrophic microglia similar to those seen in AD.
New PET Tracer Binds Muscarinic Acetylcholine Receptors
MK-6884 measures allosteric changes to the M4 subtype of muscarinic receptors in people and in monkeys. Ligand binding tightened when people took donepezil, an acetylcholinesterase inhibitor.
Identical Twins Share Tau Trajectory, but Lifestyle Can Make a Difference
Among 39 sets of identical twins, tau tangles accumulated in a strikingly similar pattern within each pair. A pair's discordance was due to Aβ and factors such as exercise.
CMS Plans to Limit Aduhelm Coverage to Clinical Trials
The decision will curtail access until efficacy is shown. Many Alzheimer’s researchers call it a reasonable compromise, others question how it will work in practice.
2021—A Turning Point for Alzheimer’s Research and Therapy?
Alzforum editors review the highlights of last year’s clinical and research developments.
In Frontotemporal Dementia Model, Do Riled-Up Microglia Help?
Progranulin deficiency hyperactivates microglia, but calming these cells worsened synapse loss and neurodegeneration in mice.
Cryo-EM Unveils Distinct Aβ42 Fibril Structures for Sporadic, Familial AD
Filaments of Aβ42 struck different poses in people with sporadic versus familial AD. The familial AD structure was also found in people with other neurodegenerative diseases, and even in APP knock-in mice.
Mighty MiGA: Microglial Genomic Atlas Zeros in on Causal AD Risk Variants
The largest transcriptomic catalogue of live microglial cells to date, MiGA cinched causal connections between genetic variation, microglial gene expression, and disease.
Does Fast-Progressing Alzheimer's Have a Whole Repertoire of Tau Conformers?
A new study claims that diverse palettes of tau species exist in the hippocampi of people with AD. Four-repeat isoforms dominated in rapidly progressing disease.
Amyloid Alone—Any Amyloid—Raises P-Tau in Mice
Cerebrospinal fluid p-tau217 and -181 rose in tandem with amyloid deposition in the brain, regardless of whether the plaques contained Aβ or amyloid formed by a different protein.
Does More Aβ38 Mean Less Cognitive Decline in Alzheimer’s?
People with subjective or mild cognitive impairment are less likely to get dementia if their CSF Aβ38 levels are high. Should γ-secretase modulators be revived?
Introducing … Sir John
Well-known to the Alzheimer’s community, John Hardy is being recognized with the knighthood in the U.K’s New Year Honours.
In Mice, Gene Editing Neutralizes Mutant APP, Keeps Plaques Away
AAV-based CRISPR snipped a piece of mutant APP and limited plaques in mice. Viruses that infiltrate only the CNS—and only neurons there—may facilitate localized gene editing in the brain.
HHS Adds Goal of Alzheimer’s Prevention to National Plan
Funding will support risk factor research and public health messaging about lifestyle modifications.
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