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Overexpressing the endosomal activator in neurons not only caused those organelles to swell, but also bungled synaptic transmission, goaded hyperphosphorylation of tau, and destroyed cholinergic neurons.
A person's blood phospho-tau level, combined with his or her APOE genotype and scores on executive function and memory tests, outperforms the clinician in predicting dementia within the next four years.
Industry analysts and watchdogs have heaped criticism on the FDA, while Alzheimer’s researchers remain divided over whether the decision helps or harms the field.
Trial data for aducanumab did not answer key questions, such as how long patients should stay on drug, leaving clinicians around the world to struggle with practical and ethical issues.
Found in one Swedish family, this mutation speeds up plaque deposition by way of two different mechanisms, leading to disease onset as young as age 40.
Amyloid Time: Because amyloid burden grows at a constant rate after having crossed a tipping point, scientists were able to predict when a person’s symptoms will begin, using only his or her age and one PET scan.
A combination of retinoic acid and the cholesterol drug gemfibrozil prompted astrocytes to ingest and degrade Aβ. Mice treated this way had fewer amyloid plaques and performed better on cognitive tests.
In Lewy body dementia brain tissue, CD4+ T cells loitered near synuclein aggregates and dopaminergic neurons. In vitro, T cells reacted to α-synuclein fragments by spewing the pro-inflammatory cytokine interleukin 17A.
Courtesy of one changed amino acid, human microglia resist drugs that typically destroy them. The cells behave normally and replenish endogenous mouse microglia
Summoned by microglia, T cells trigger neurodegeneration in a mouse model of tauopathy. Does this happen in Alzheimer’s disease?
An amino acid change in this ApoE receptor-binding protein may have bestowed 20 years of resilience to a brother and sister carrying the presenilin Paisa mutation.
Arranged in bundles and lattices within a plaque, Aβ42 fibrils were intermixed with extracellular vesicles of different shapes and sizes. Their origin remains unknown.
A postmortem study found that people who had more aggregation-prone, hyperphosphorylated, oligomeric forms of tau in their brains also had a more aggressive form of Alzheimer’s disease during life. Will we personalize tauopathy care like cancer care?
Experts say the low specificity of Quest Diagnostics’ plasma Aβ test could lead to more false than true positives, causing distress and confusion.
Big data analyses correlate viral load with clinical, molecular, and pathological features of AD. Time to consider the pathogen hypothesis anew?
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