In Pilot Study, Electric Therapy Improves Memory
Sending low-intensity, gamma frequency electric current through the brain boosted short-term memory, perhaps by increasing cholinergic transmission.
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Sending low-intensity, gamma frequency electric current through the brain boosted short-term memory, perhaps by increasing cholinergic transmission.
In postmortem brain, proteins involved in all manner of vesicular functions waxed or waned with increasing phases of disease, starting years prior to symptoms.
A new trial will compare digital and blood-based biomarkers to amyloid PET scans in order to learn which ones best pick out early plaque accumulation.
People who develop Type 2 diabetes before age 60 have more than double the dementia risk, and earlier dementia onset, than those without diabetes.
The fewer their meningeal lymphatic vessels, the slower treated mice clear plaques. Lymphatic dysfunction also drives microglial activation, hinting at a role in pathology.
Machine learning analysis of 912 PET scans says neurofibrillary tangles spread through the AD brain in one of four distinct patterns.
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.
In mice, an IgG4 version of semorinemab better protected neurons, but for AX004, an IgG1 version better cleared tau. How to make the choice?
In animals, polyamines such as spermidine enhance autophagy, rejuvenate mitochondria, and slow cognitive decline. Buzzword: hypusination. Human data not far behind.
In mice, polyamines boost autophagy and promote clearance of soluble Aβ species. In cells, they counteract tau aggregation. In the Alzheimer’s brain, their metabolism is ramped up. Could spermidine supplements prevent or treat AD?
Certain neurons crank up ApoE expression with age in mice. Ditto with AD progression in people. These same neurons ramp up immune response genes. The shift could foreshadow their demise.
A “mammalian-wide interspersed repeat-natural antisense transcript” blocks translation of tau mRNA. Other MIR-NATS may act on α-synuclein and APP.
Downregulation of a chemokine receptor traps T cells in the meninges. Glymph drainage slows, amyloid burden rises.
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.
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