Blood samples taken from people enrolled in an Alzheimer's research study revealed higher levels of phosphorylated tau 217 that correlated with the presence of amyloid plaques. People with amyloid in their brains had up to three times more of the tau protein in their blood than those who had no evidence of amyloid accumulation. The higher levels of the protein were evident even in people with no signs of cognitive decline.
Animal study reveals the formation of amyloid plaques drives brain tissue loss and neurodegeneration in Alzheimer's disease. However, lithium, a drug commonly used to treat bipolar disorder, reduces the life-shortening effects of the loss.
Amyloid accumulation occurs faster in those who have objectively-defined cognitive difficulties than older people who are considered to be cognitively normal. Mild cognitive impairment is also associated with faster hippocampal and entorhinal cortex atrophy.
Subtle changes in thinking and memory may appear before, or in conjunction with, the development of amyloid plaques.
Researchers use SWITCH technology to label amyloid plaques in mouse models of Alzheimer's disease so they could be imaged in fine detail at different ages. They were consistently able to see the plaques first emerged in deep brain structures and tracked circuits, such as the Papez memory circuit, to spread throughout the brain as the animal aged.
Researchers map a toxic protein associated with Alzheimer's disease. The study reports that pS8-AB40 acts as the alpha structure in polymorphism and has higher levels of cellular toxicity compared to other fibrils.
Inducing gamma oscillations with visual stimulation via a process known as gamma entrainment using sensory stimuli, or GENUS, was shown to reduce amyloid plaques and phosphorylated tau in mouse models of dementia. Providing GENUS daily during the early stages of neurodegeneration helps preserve neural and synaptic density across multiple brain areas and improves cognitive performance for learning and spatial memory tasks.
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Axon myelination is significantly disrupted in patients with Alzheimer's disease. Researchers also found brain cells of men and women vary significantly in how their genes respond to the neurodegenerative disease.
Depleting BACE1 completely reverses the formation of amyloid plaques and improves cognitive function in mouse models of Alzheimer's disease, researchers report.
A new study that analyzed the brains of 107 older people sheds light on the neurobiology of both healthy and diseases aging.
According to researchers, the compound P7C3 may help to protect against neuron death and memory problems associated with Alzheimer's disease without altering the buildup of amyloid plaques or neurofibrillary tangles in rat brains.