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.
APP found to also be involved in neurogenesis
A new function has been found for the amyloid precursor protein (APP), which may help explain how it goes awry in Alzheimer's disease. It appears that APP (which is involved in the creation of amyloid-beta), also helps control the growth and maturation of newborn brain cells, by regulating a specific microRNA (microRNA-574-5p) that normally promotes neurogenesis.
http://www.eurekalert.org/pub_releases/2014-04/s-nrd041814.php
Hippocampal iron increased in Alzheimer's disease
The hippocampus is damaged early in Alzheimer’s, while the thalamus is generally unaffected until the late stages. Brain imaging of the hippocampus and the thalamus in 31 patients with Alzheimer's and 68 healthy controls has revealed increased levels of iron in the hippocampus of those with Alzheimer’s, but not in the thalamus. Moreover, this increased iron was associated with tissue damage in patients with Alzheimer's but not in the healthy older individuals.
Individual differences in Alzheimer's molecular structure
The first detailed characterization of the molecular structures of amyloid-beta fibrils that develop in the brains of those with Alzheimer's disease suggests that different molecular structures of amyloid-beta fibrils may distinguish the brains of Alzheimer's patients with different clinical histories and degrees of brain damage.
Genes involved in familial Alzheimer's disease
Understanding a protein's role in familial Alzheimer's disease
Genetic engineering of human induced pluripotent stem cells has revealed very specifically how a key mutated protein is involved in familial Alzheimer's. Familial Alzheimer’s is a subset of early-onset Alzheimer's disease that is caused by inherited gene mutations.
Researchers classify Alzheimer's patients in 6 subgroups
A study involving 4,050 people with late-onset Alzheimer's disease (mean age 80) has classified them into six groups based on their cognitive functioning at the time of diagnosis. A genetic study found two of the groups showed strong genetic associations.
Brain blood flow deficits in Alzheimer's explained
It’s been known that decreased blood flow in the brain occurs in people with Alzheimer's, and recent studies suggest that brain blood flow deficits are one of the earliest detectable symptoms of dementia. A study has now shown why it occurs: a small percentage of capillaries, the smallest blood vessels in the brain, are blocked by white blood cells stuck to the inside of the capillaries.
Recent research has shown that capilleries are vital for monitoring and directing blood flow around the brain.
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.
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