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In the Finnish city of Kuopio, surgeons and scientists have built a unique protocol. It improves life for people with hydrocephalus—and it banks cortical tissue rife with preclinical pathology and gene variants for Alzheimer's research.
In the Finnish city of Kuopio, neurosurgeons collaborate with neurophysiologists and molecular and cellular biologists to make frontal cortex, dura, intraventricular CSF, skin, fat, and other tissue from hydrocephalus patients available for research purpo
A new method for precisely localizing pathological tau in whole mouse brain finds that its spread follows network connections—but it seems to move up axons, not down.
In mice with amyloidosis, removal of miR-155 from microglia rendered the cells more receptive to IFN-γ stimulation, improving neuroprotection.
The Elecsys-based assay could run on 100,000 fully automated diagnostic machines worldwide.
In a small open-label Phase 1/2 trial, Denali’s enzyme replacement therapy lowered neurofilament light in the cerebrospinal fluid by half and in serum by two-thirds.
New studies report that transdifferentiated neurons from AD patients retain signatures of aging. They also model lysosomal dysfunction, tau phosphorylation, and cell death.
Cells of the neurovascular unit upregulate inflammation-related genes and stifle genes of the blood-brain barrier. The genes include 125 known to carry AD risk variants.
Feeding taurine to mice and monkeys increased the lifespan of the former and reduced signs of aging in both.
Known for his work on animal models, APP processing, and the cholinergic system, Price founded one of the first Alzheimer’s Disease Research Centers.
In cognitively unimpaired older adults, some gut bacteria correlated with plaques and tangles, but not neurodegeneration.
A giant of basic science, Ihara biochemically characterized Aβ and tau deposits in AD brain, laying the groundwork for subsequent discoveries.
The panel was persuaded of the antibody’s clinical efficacy and overall favorable benefit/risk ratio, although it had questions about risk in certain subgroups.
In VSP35 knockout cells, surface proteins get trapped in endolysosomes. They swell with undigested proteins and APP, then spew their contents outside the cell.
In amyloidosis mice, decline of the hypothalamic melanin-concentrating hormone system jacks up neuronal activity, and contributes to sleep problems.
