Lipid-Laden, Sluggish Microglia? Blame Aβ.
Droplets of triglycerides accumulate in microglia exposed to Aβ fibrils. These cells barely ate Aβ, and released molecules that damage neurons.
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Droplets of triglycerides accumulate in microglia exposed to Aβ fibrils. These cells barely ate Aβ, and released molecules that damage neurons.
Together, the two immune-cell types deal a neurodegenerative blow more powerful than either can inflict alone.
Compared to AD, tau tangles in PART accumulated slowly, and only in the medial temporal lobe. Cognition slipped subtly, and no amyloid amassed over three years.
Experts say the low specificity of Quest Diagnostics’ plasma Aβ test could lead to more false than true positives, causing distress and confusion.
Proteins involved in the extracellular matrix, metabolism, immunity, proteostasis, and synaptic function change in the CSF and plasma up to 30 years before dementia sets in.
Few people with Down's syndrome have cardiovascular risk factors, yet most develop cerebrovascular disease. Will this complicate anti-amyloid immunotherapy?
Two men with loss-of-function variants in their APOE4 alleles escaped amyloid pathology. One was in his 90s.
Swapping allele expression in astrocytes lowered amyloid load, lessened gliosis, and improved memory. This works even after amyloidosis is in full swing.
Scientists at AAIC debated discrepant results, updated a model of the biomarker-efficacy relationship, and debuted the CenTauR scale for tau PET.
At AAIC 2023, scientists tied clinical success to drug exposure, speed of plaque clearance, amyloid negativity.
DNA from leaky mitochondria unleash the cGAS-STING cascade, triggering interferon responses in the brain.
A section of the protein folds on itself to form five layers. Three V-shaped layers cradle each other. This differs from the double-spiral fold in people with FTD/ALS.
The newly proposed scheme uses only amyloid and tau for diagnosis and staging. It establishes parallel tracks for fluid or imaging markers, and recognizes a clinical stage zero.
α-Synuclein seed amplification assays identify people with LBD. They may outperform clinical diagnosis, and hint that dementia with Lewy bodies might be overdiagnosed.
Twelve people heterozygous for this protective variant were still sharp seven years after their expected age of AD onset. One had fewer tangles than expected.