Does Calcium Overload Mark Dendritic Spines for Destruction?
In a mouse model of cortical multiple sclerosis, microglia and monocytes swooped in to gobble up synapses when dendritic calcium rose. Spines grew back once inflammation subsided.
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In a mouse model of cortical multiple sclerosis, microglia and monocytes swooped in to gobble up synapses when dendritic calcium rose. Spines grew back once inflammation subsided.
Some people with severe COVID-19 have neurovascular injury and elevated markers of neural damage in their blood and CSF. What’s going on in their brains?
Plaque-ridden 5xFAD mice were no better at fending off an intracerebral herpes virus infection than their wild-type counterparts. The virus was not to be found within Aβ plaques and did not spur plaques to form.
Researchers identified genetic variants that may explain why some ApoE4 carriers remain free of Alzheimer’s, while some ApoE2 carriers do not.
Scientists at the AAT-AD/PD conference debuted new detection methods for this biomarker, which they say distinguished healthy controls from MCI and AD.
Assays will help doctors diagnose Alzheimer’s disease and amnestic mild cognitive impairment in Taiwanese clinics.
Besides the big-gun antibodies and BACE inhibitors, smaller, lesser-known drug programs are inching their way through the clinical trials pipeline. As is often the case, Phase 1 seems encouraging.
Despite plaques and tangles in the brain, this group, on average, maintains their cognitive skills over two to four years, suggesting the presence of resilience factors.
In response to an FDA request, the drug’s sponsor submitted new data analyses. The agency moved the action date to June 7.
In a career spanning four decades, Davies spearheaded the cholinergic hypothesis, unlocked secrets of tau, and readily shared antibodies in the field.
Mutated huntingtin may stow away in synaptic vesicles to sneak from one neuron to another.
Conformations of misfolded tau survive injection from one mouse to the next, a property shared by prions.
People who report not participating in social or cognitive activities are more likely to develop dementia within the next few years, but not after that. The findings cast nonparticipation as a consequence, not a cause, of neurodegeneration.
In mouse brain slices at least, tau shuffles in and out of protein inclusions. The tangles grew more inert as the tissue aged.
Sensor algorithms can accurately capture patterns of resting tremor and dyskinesia. This could help clinicians manage symptoms and medication.