Proteomics Dates Endosomal, Synaptic Changes to Preclinical AD
In postmortem brain, proteins involved in all manner of vesicular functions waxed or waned with increasing phases of disease, starting years prior to symptoms.
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In postmortem brain, proteins involved in all manner of vesicular functions waxed or waned with increasing phases of disease, starting years prior to symptoms.
The iPSC Neurodegenerative Disease Initiative is creating 100+ isogenic cell lines. Each carries a different risk variant for Alzheimer's or a related dementia. Scientists around the world can obtain the cells through Jackson Labs.
The first detailed look at expression profiles in blood vessels of the human brain identifies new cell subtypes. These cells express 30 of the top 45 AD risk genes.
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?
In the Alzheimer’s brain, too, plaques trigger a coordinated inflammatory response from microglia and astrocytes. A preprint paper had shown the same for mice.
The more a person’s gut microbiome becomes individualized with age, the longer that person's lifespan and the better his or her health, say scientists.
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In stark contrast to Aβ and tau fibrils, α-synuclein fibrils are asymmetric, comprising two different protofibrils.
Umbilical cord stem cells from presenilin 1 E280A carriers, once differentiated into cholinergic-like neurons, pumped out Aβ42 and accumulated phosphorylated tau and apoptotic markers.
Induced neurons lacking the Alzheimer’s risk gene can’t properly recycle APP.
In cell culture, slashing Aβ production by more than half harmed neuronal signaling, but a smaller cut maintained it.
New research suggests the R47H variant protects neurons from neurodegeneration, raising questions about staging and direction of future TREM2-based therapy.
By suppressing a single gene, scientists triggered the transformation of astrocytes into neurons in the mouse substantia nigra, where the converts released dopamine and connected with the striatum.
A mouse study claims that the small GTPase restrains pro-inflammatory responses in microglia. Aβ oligomers inhibit RhoA, promoting Aβ deposition and neurodegeneration.
Released from hippocampal neurons in response to experience, the cytokine prompted microglia to eat extracellular matrix around synapses. This facilitated growth of new spines, and sharpened memory.