Are Mid-Life Depression and Anxiety Early Signs of Alzheimer’s?
CSF Aβ and tau are abnormal in older people with psychiatric problems. Are these symptoms an effect of AD pathogenesis, or risk factors for it?
6538 RESULTS
Sort By:
CSF Aβ and tau are abnormal in older people with psychiatric problems. Are these symptoms an effect of AD pathogenesis, or risk factors for it?
In a career that spanned more than 40 years, Trojanowski broadened and deepened the field's understanding of the molecular pathology of neurodegenerative diseases.
A person's burden and spatial distribution of plaques, as measured by PiB-PET, varied greatly depending on his or her mutation. Their CSF Aβ42 or cognitive decline did not.
APP or presenilin mutation carriers who also carried the Met66 allele had more p-tau217 at presymptomatic stages, and more p-tau205 at symptomatic stages, than did Val carriers.
Large multinational meta-analysis also found that among people without dementia, CSF Aβ42 edged out PET in detecting amyloid pathology.
Certain MHC class II subtypes reduce a person’s risk of Alzheimer's and Parkinson's. They bind an acetylated snippet of tau.
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.
No filters selected