Healthy, Drug-Resistant Microglia Reinvigorate Mouse Brain
Courtesy of one changed amino acid, human microglia resist drugs that typically destroy them. The cells behave normally and replenish endogenous mouse microglia
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Courtesy of one changed amino acid, human microglia resist drugs that typically destroy them. The cells behave normally and replenish endogenous mouse microglia
In a 45-page report, two House committees rebuked the agency for working too closely with drug sponsor Biogen.
A collection of antibodies against microglial proteins is starting off a new database on Alzforum.
In some patients, the blood Aβ42/40 test fell too close to the cutoff for specialists to confidently diagnose AD. Comorbidities, drugs also complicate results. Two CSF tests are FDA-approved.
Plasma p-tau climbs as bears sleep. Post-torpor, tau reverts to normal. Does neuronal metabolic activity have to do with it?
Brain-derived forms of tau distinguished people with Alzheimer's from those with other neurodegenerative diseases.
Mirroring earlier results, a larger study finds that high levels of this tau fragment in CSF tracked with neurofibrillary tangles, but not amyloid plaques.
Antemortem plasma p-tau217 predicted the extent of amyloid plaques and neurofibrillary tangles seen postmortem.
In some patients, the blood Aβ42/40 test fell too close to the cutoff for specialists to confidently diagnose AD. Comorbidities, drugs also complicate results. Two CSF tests are FDA-approved.
CSF monocytes increasingly crank out the chemokine CXCL16, while T cells up its receptor, CXCR6. The same cross-talk unfolded among microglia and T cells around plaques.
The assay captures α-sheet structure. It detected AD with 99 percent accuracy, including among healthy people who later became cognitively impaired.
The more foliage near a person’s residence, the less likely they are to have either disease.
In a small pilot study, tailoring lifestyle changes to the individual boosted cognition, with an effect size three times that seen in the Finger trial.
In the Graduate trials, the anti-amyloid antibody gantenerumab cleared only half as much plaque as it had done in earlier studies. Is formulation or dosing to blame?
Conformers amplified from CSF of late-stage PD adopt distinct folds and trouble neurons.
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