Link found between Alzheimer’s disease biomarkers in healthy adults
A University of Iowa study provides insight into a calcium-sensing enzyme already known to play a role in irregular heartbeats and other critical functions. The researchers showed that the enzyme, calmodulin kinase II (CaM kinase II), contributes to arrhythmia in an extremely rare disease called Timothy syndrome and that inhibiting the enzyme prevents irregular heartbeats.
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A study published in the November issue of the Journal of Alzheimer’s Disease provides an insight into normal, physiological levels and association between proteins involved in development of Alzheimer’s disease.
A group of scientists and physicians from the University of Washington and Puget Sound Veterans’ Affairs Health Care System in Seattle, in collaboration with groups from the University of Pennsylvania and the University of California San Diego, performed a study in cognitively normal and generally healthy adults, from young to old (age range 21-88 years), of both genders, measuring levels of different brain-derived molecules associated with Alzheimer’s disease.
Investigators determined that cerebrospinal fluid (CSF) levels of apolipoprotein E (apoE), one of the most important proteins involved in transfer of fatty substances between different brain cells, are highly correlated with the levels of proteins known to be involved in development of Alzheimer’s disease, amyloid precursor protein (APP) and tau. While many studies have previously shown that apoE gene is very important for Alzheimer’s disease development, the connection between apoE protein and other relevant CSF markers in healthy adults was not known. Although this type of study cannot establish causal associations, the results strongly suggest that the CSF levels of apoE may explain a significant proportion of the levels of APP- and tau-related biological markers in the healthy human brain, indicating a strong physiological link between apoE, APP and tau. In other words, the study points to a possibility that modulation of the levels of apoE may affect the levels of APP and tau in the brain.
Furthermore, the study has shown that people who have a “beneficial” genetic form of apoE (so-called APOE2), which is associated with lower risk of Alzheimer’s disease, have lower CSF levels of beta-amyloid peptide 42, a molecule implicated in development of Alzheimer’s disease plaques. This finding may explain some of the basis for the known protective effects of the APOE2 observed in large population studies.
Dr. Simona Vuletic, Northwest Lipid Metabolism and Diabetes Research Laboratories, University of Washington School of Medicine, Seattle, commented, “Understanding the associations between these important molecules in the brain of cognitively normal, healthy people will help us develop better strategies not only for diagnosis, but possibly also better prevention and treatment for Alzheimer’s disease. This study also provides baseline data and an opportunity to understand how these normal relationships change, leading to the disease.”
The only known genetic risk factor for Alzheimer’s disease slows down the brain’s ability to export a toxic protein known as amyloid-beta that is central to the damage the disease causes, scientists have found. The research, published Nov. 13 by the Journal of Clinical Investigation, provides new clues into the workings of a protein known
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Mice that were fed a diet rich in fat, sugar and cholesterol for nine months developed a preliminary stage of the morbid irregularities that form in the brains of Alzheimer’s patients. The study results, published in a doctoral thesis from the Swedish medical university Karolinska Institutet (KI), give some indications of how this difficult to
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Swedish research has found a link between fast food and Alzheimer’s disease. The research by scientists at the Karolinska Institutet has revealed that mice fed a diet of junk food for a nine month period developed the abnormal brain tangles which are seen in the preliminary stages of Alzheimer’s disease - they say a
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Researchers have found that two proteins which work in tandem in the brain’s blood vessels present a double whammy in Alzheimer’s disease. Not only do the proteins lessen blood flow in the brain, but they also reduce the rate at which the brain is able to remove amyloid beta, the protein that builds up in
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UCLA scientists have used innovative brain-scan technology developed at UCLA, along with patient-specific information on Alzheimer’s disease risk, to help diagnose brain aging, often before symptoms appear. Published in the January issue of Archives of General Psychiatry, their study may offer a more accurate method for tracking brain aging. Researchers used positron emission tomography (PET),
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