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Mechanism of site-specific tau phosphorylation linked to Alzheimers Disease-related hyperphosphorylation defines master sites that govern phosphorylation across the entire tau molecule
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A-beta 1-40 builds up in the walls of pial arteries (that control the supply of blood and oxygen) and reduces blood flow to the brain, causing memory loss.
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An organelle may target tau degradation
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Synaptic connections restored in mouse model of Alzheimers when given the drug known as Silent Allosteric Modulation or SAM
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Changes in FMNL2 activity caused by cerebrovascular disease prevent the efficient clearance of toxic proteins from the brain, eventually leading to Alzheimer’s disease
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Vitamin D deficiency associated with neuroimaging outcomes and the risks of dementia and stroke
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A Single Molecule May Result in Alzheimers
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Association between physical activity and risk of depression
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An antidepressant mechanism for psilocybin therapy: global increases in brain network integration
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Microglia: The Significance of States and Fates
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New insights into the genetic etiology of Alzheimers disease and related dementias
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A computational model of neurodegeneration in Alzheimers disease
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FDA-approved drug shows improved cognitive function in people with Alzheimers Disease and a mouse model of Down syndrome
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Four genes (TMEM106B, RAB27B, GMPPB, and NEGR1) affect depression by influencing protein and gene expression level
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Neurons detect cognitive boundaries to structure episodic memories in humans
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Sauna-like conditions or menthol treatment reduce tau phosphorylation through mild hyperthermia
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Directed Antibodies to NMDA Receptors May Thwart Neurodegeneration
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Antidepressant effects of psilocybin-assisted therapy may be durable at least through 12months