Proteomics Highlight Alzheimer’s Changes in Matrisome, MAPK Signaling
Protein networks unseen in RNA data correlated closely with plaques, tangles, cognitive decline. Many are in the extracellular matrix.
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Protein networks unseen in RNA data correlated closely with plaques, tangles, cognitive decline. Many are in the extracellular matrix.
Dementia risk nearly doubled after each minor stroke and tripled after each major one, regardless of vascular risk factors. Risk climbed almost sevenfold after multiple major strokes.
An unbiased “interactome” generated from human neurons could shed light on what goes wrong in tauopathies, and help identify new therapeutic targets.
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.
MK-6884 measures allosteric changes to the M4 subtype of muscarinic receptors. Ligand binding tightened when people took donepezil, an acetylcholinesterase inhibitor.
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.
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.
Alzforum editors review the highlights of last year’s clinical and research developments.
Progranulin deficiency hyperactivates microglia, but calming these cells worsened synapse loss and neurodegeneration in mice.
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.
The largest transcriptomic catalogue of live microglial cells to date, MiGA cinched causal connections between genetic variation, microglial gene expression, and disease.
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.
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.
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?
Well-known to the Alzheimer’s community, John Hardy is being recognized with the knighthood in the U.K’s New Year Honours.
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