Moving Alzheimer’s Diagnosis to Primary Care Could Ease Bottlenecks
A Rand report concludes that using blood-based biomarkers and cognitive tests in primary care would halve wait times for new disease-modifying therapies.
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A Rand report concludes that using blood-based biomarkers and cognitive tests in primary care would halve wait times for new disease-modifying therapies.
With newly available fluid biomarkers that detect α-synuclein pathology in the brain, researchers articulate ways to classify the disease based on its biology.
Antemortem plasma p-tau217 predicted the extent of amyloid plaques and neurofibrillary tangles seen postmortem.
In more than 52,000 cognitively healthy people, elevated plasma GFAP or NfL more than doubled the risk the person would develop dementia over the next 14 years.
Layer 1 interneurons vanish. Layer 2/3 excitatory neurons become hyperactive, then fade. Microglia change state. Astrocytes react. No symptoms yet. Is this preclinical Alzheimer's?
£50 million in funding will expand trial access, increase recruitment, streamline study processes, and train staff over the next five years.
Methylated CAG-repeat RNAs and 14-3-3θ promote TDP-43 aggregation.
Lamivudine slightly improved markers of astrogliosis and amyloid pathology. The drug suppresses activity of retrotransposons that are under-methylated in AD.
In APOE4/4 microglia, Aβ triggers an uptick of a triglyceride synthesis enzyme. The cells then accumulate lipid droplets and release something neurotoxic.
O-GlcNAcase inhibitors and a vaccine head to Phase 2. New antibody strategies co-opt the proteasome to clear intracellular and extracellular tau in preclinical models.
Researchers at AD/PD showcased progress in modeling these conditions, detecting CAA, and potentially mitigating microhemorrhages.
Knocking down these capillary-hugging cells triggers a domino effect; blood proteins invade the brain, white matter deteriorates, and neurons die.
In the field's quest for disease-modifying treatments, two different α-synuclein vaccines and two antibodies look promising in preclinical studies, as well.
With effective symptomatic treatments in hand, many Parkinson’s researchers have now set their sights on loftier goals...
At AD/PD, scientists presented small molecules that break up fibrils and antibodies that target pathogenic forms of α-synuclein or hinder spread in iPSCs and mice.
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