While everyone agrees that amyloid-beta protein is part of the problem, not everyone agrees that amyloid plaques are the cause (or one of them) of Alzheimer’s. Other forms of amyloid-beta have been pointed to, including floating clumps called oligomers or ADDLs. A new study, using mice engineered to form only these oligomers, and never any plaques, throughout their lives, provides more support for this theory. Mice that never developed plaques were just as impaired by the disease as mice with both plaques and oligomers, and when a gene that converted oligomers into plaques was added to the mice, the mice were no more impaired than they had been before. This may explain why treatments aimed at removing plaques have not been successful, and offers a new approach to the treatment of Alzheimer’s.
Alzheimer's memory problems originate with oligomers not plaques
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Low levels of omega-3 fatty acid may contribute to Alzheimer’s
Low levels of DHA, an omega-3 fatty acid, have been found in the brains of those with Alzheimer's disease, but the reason has not been known. A new study has found that lower levels of DHA in the liver (where most brain DHA is manufactured) were correlated with greater cognitive problems in the Alzheimer’s patients. Moreover, comparison of postmortem livers from Alzheimer’s patients and controls found reduced expression of a protein that converts a precursor acid into DHA, meaning the liver was less able to make DHA from food.
Link among Alzheimer's disease, Down syndrome, atherosclerosis and diabetes
It’s been suggested before that Down syndrome and Alzheimer's are connected. Similarly, there has been evidence for connections between diabetes and Alzheimer’s, and cardiovascular disease and Alzheimer’s. Now new evidence shows that all of these share a common disease mechanism. According to animal and cell-culture studies, it seems all Alzheimer's disease patients harbor some cells with three copies of chromosome 21, known as trisomy 21, instead of the usual two. Trisomy 21 is characteristic of all the cells in people with Down syndrome.
How inflammation and hypoxia damage the brain
A new study shows that a combination of inflammation and hypoxia activates microglia in a way that persistently weakens the connection between neurons, contributing to brain damage in conditions such as stroke and Alzheimer's disease.
http://www.eurekalert.org/pub_releases/2014-03/uobc-scb031214.php
Importance of vascular factors in Alzheimer's disease
Analysis of 5715 cases from the National Alzheimer's Coordinating Center (NACC) database has found that nearly 80% of more than 4600 Alzheimer's disease patients showed some degree of vascular pathology, compared with 67% of the controls, and 66% in the Parkinson's group. The link was especially strong for younger patients with Alzheimer’s.
Brain network decay detected in early Alzheimer's
A multi-year study involving 207 healthy older adults, in which their spinal fluids were repeatedly sampled and their brains repeatedly scanned, has found that disruptions in the default mode network emerges about the same time as chemical markers of Alzheimer’s appear in the spinal fluid (decreased amyloid-beta and increased tau protein). The finding suggests not only that amyloid-beta and tau pathology affect default mode network integrity early on, but that scans of brain networks may be an equally effective and less invasive way to detect early disease.
Inflamed iron-containing cells found in Alzheimer's brains
A post-mortem study of five Alzheimer's and five control brains has revealed the presence of iron-containing microglia in the subiculum of the Alzheimer's brains only. The subiculum lies within the hippocampus, a vital memory region affected early in Alzheimer's. None of the brains of those not diagnosed with Alzheimer's had the iron deposits or the microglia, in that brain region, while four of the five Alzheimer's brains contained the iron-containing microglia.
Impaired waste management in the brain a cause of Alzheimer's?
Aging linked to impaired garbage collection in the brain
A mouse study has shown that, as cells age, their ability to remove damaged proteins and structures declines.
The process of waste management, called autophagy, involves a component within the cell (an autophagosome) engulfing misfolded proteins or damaged structures (putting them in a garbage bag, essentially). The autophagosome then fuses with a second cellular structure, called a lysosome, that contains the enzymes needed to breakdown the garbage, allowing the components to be recycled and reused.
Blood-clotting protein implicated in cognitive decline and Alzheimer's
Alzheimer's disease is associated with abnormalities in the vast network of blood vessels in the brain, but it hasn’t been known how this affects cognition. A study has now shown that a blood-clotting protein called fibrinogen plays a part.
The study found that fibrinogen, after leaking from the blood into the brain, activates the brain's immune cells and triggers them to destroy synapses, which are critical for neuronal communication.
Tau protein travels with neuronal signals
Tau protein stabilizes structures that transport supplies from the center of the cell to the extremities, but sometimes some tau is not bound to these microtubules and instead clumps together into neurofibrillary tangles — one of the hallmarks of Alzheimer's disease, and also linked to other neurodegenerative disorders. A new study supports the theory that ‘bad’ tau travels to different brain regions via the synapses — that is, it’s secreted with the signals passing between neurons.
Where Alzheimer's starts and how it spreads
A new study involving 96 older adults initially free of dementia at the time of enrollment, of whom 12 subsequently developed mild Alzheimer’s, has clarified three fundamental issues about Alzheimer's: where it starts, why it starts there, and how it spreads.
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