Sans Microglia, Mice Develop CAA and Die Young
5xFAD mice lacking microglia develop cerebral amyloid angiopathy and amass calcium deposits. Most die by 6 months old.
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5xFAD mice lacking microglia develop cerebral amyloid angiopathy and amass calcium deposits. Most die by 6 months old.
Limbic-predominant age-related TDP-43 encephalopathy (LATE) most often co-occurred with AD pathology, but was detected on its own as well.
α-Synuclein prevents de-capping of transcripts, hindering their turnover. In human brain, α-synuclein accumulation correlated with slower mRNA decay.
TDP-43 inclusions in intramuscular nerve bundles, paired with clinical criteria, may enable diagnoses at early stages of ALS.
A case-control study of half a million people nabbed the variants. Both are rare, lie in the C-terminal lipid-binding domain, and one neutralizes ApoE4.
In two Phase 1 trials, DNL201 reduced LRRK2 kinase activity in blood mononuclear cells. The inhibitor reached the same level in CSF as in blood. There were no serious side effects.
Months before mice develop plaques, faulty lysosomes swollen with Aβ commandeer plasma, ER, and Golgi membranes, creating toxic rosettes around the nucleus. The neurons eventually burst, leaving behind plaques.
Adeno-associated viruses carrying Cas9 and guide RNAs cut hexanucleotide repeats out of the C9ORF gene. RNA inclusions and poly-dipeptides became sparse.
The actin-binding protein associated with tau aggregates in people with PSP, and rare variants in the gene associated with the disease.
A provocative new study suggests that unlike in mice, TSPO in people does not rise with microglial activation; instead, a higher PET signal reflects more microglia.
Proteins stuck around longer in the oldest mice. Those involved in neurodegeneration had the most extended lifespans.
The first FDA approval of a CSF test, and increased options for plasma testing, will give patients easier access to these diagnostic aids. Will physicians interpret them properly?
The Aβ oligomer-busting peptide RD2 cleared protofibrils in extracts from both.
CSF from young mice or young people revved oligodendrogenesis and myelination, thanks in part to a growth factor.
A population of AGTR1-expressing dopaminergic neurons in the ventral slice of the human substantia nigra were selectively vulnerable in Parkinson's disease. These cells also expressed the most PD risk genes.