Remember Amyloid-eta? A Decade Later, News on a Physiological Function
To modulate synapses, Aη weakens ion flux through glutamate receptors and strengthens their non-ionotropic signaling. This dual action is a first, say scientists.
To modulate synapses, Aη weakens ion flux through glutamate receptors and strengthens their non-ionotropic signaling. This dual action is a first, say scientists.
In mouse models of amyloidosis, CD8+ T cells trigger myelin pathology by rousing microglia and confusing oligodendrocytes.
Mice missing microglia develop astrogliosis and neurodegeneration by middle age. Giving them healthy microglia prevents or reverses pathology.
Nixing an endosomal targeting sequence shields APP from BACE1, reducing Aβ and pathologic C-terminal fragments in mice.
Injected into the cerebrospinal fluid, a viral vector delivers the lysosomal protein into the human brain. In mice, a protein transport vehicle delivered into the blood does the same.
A panel of eight plasma proteins identified people who were on the path to Parkinson’s. Could this help select participants for prevention trials?
With limited guidance, physicians will have to navigate questions about whom to treat, when to stop, and how to manage safety.
People who sifted through piles of debris are nine times likelier to develop early onset, all-cause dementia than those exposed to little toxic dust.
After infiltrating the brain in mouse models of amyloidosis, peripheral T cells send microglia and oligodendrocytes into a tizzy, creating a myelin mess in the process, according to new data. Scientists report that CD8+ T cells stir a subset of interferon-γ-responsive microglia, break up myelin, and hinder repair by oligodendrocytes. Knocking down the CD8+ T cells or microglia preserved myelin and memory. These results support the idea that infiltrating T cells contribute to a neurodegenerative environment in Alzheimer’s disease.
Could replacing dysfunctional microglia with healthy versions prevent or even reverse pathology in microglial diseases? Two papers suggest as much. In both, mice lacking microglia develop astrogliosis, reactive oligodendrocytes, neurodegeneration, white-matter atrophy and calcification, symptoms of leukoencephalopathy. Adding healthy mouse or human microglia into the brains of the mice resolved most of the pathologies. Could microglial transplantation become a therapy?
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