According to a study published Online First by Archives of Neurology, one of the JAMA/Archives journals, researchers from the University of California, San Diego, have found no association between an antioxidant combination of vitamin E, vitamin C and Î -lipoic acid (E/C/ALA) and changes in some cerebrospinal fluid biomarkers related to Alzheimer's disease. In the brain, oxidative impairment is linked to aging and is common in individuals with Alzheimer's disease (AD). Even though some studies have indicated that a diet rich in antioxidants may lower the risk of developing AD, results from antioxidant studies in AD have been mixed. Douglas R. Galasko, M.D., of the University of California, San Diego, and his team enrolled 78 patients from the Alzheimer's Disease Cooperative Study (ADCS) Antioxidant Biomarker study in order to analyze alterations in cerebrospinal fluid (CSP) biomarkers associated to AD and oxidative stress, function and cognition.
The March 22 issue of Neuron reveals that a newly developed mathematical computer program has tracked the manner in which different forms of dementia spread within a human brain, and that it can predict where and approximately when the spread occurs in a patient's brain neuron to neuron of 'prion-like' toxic proteins, which is the same process on which all forms of dementia are based. Patients and their families could benefit from the findings by being helped to confirm a diagnosis of dementia, which would also enable them to prepare ahead for future cognitive declines that will happen over time. According to lead researcher, Ashish Raj, the program may in the future also assist physicians in identifying suitable brain targets for therapeutic interventions, in a time where targeted drugs against dementia already exist.
Just as the familiar sugar in food can be bad for the teeth and waistline, another sugar has been implicated as a health menace and blocking its action may have benefits that include improving long-term memory in older people and treating cancer. Progress toward finding such a blocker for the sugar - with the appropriately malicious-sounding name "oh-glick-nack" - was the topic of a report at the 243rd National Meeting & Exposition of the American Chemical Society (ACS), the world's largest scientific society. Linda Hsieh-Wilson, Ph.D., explained that the sugar is not table sugar (sucrose), but one of many other substances produced in the body's cells that qualify as sugars from a chemical standpoint. Named O-linked beta-N-acetylglucosamine - or "O-GlcNAc" - it helps in orchestrating health and disease at their origins, inside the billions of cells that make up the body.
Insulin resistance in the brain precedes and contributes to cognitive decline above and beyond other known causes of Alzheimer's disease, according to a new study by researchers from the Perelman School of Medicine at the University of Pennsylvania. Insulin is an important hormone in many bodily functions, including the health of brain cells. The team identified extensive abnormalities in the activity of two major signaling pathways for insulin and insulin-like growth factor in non-diabetic people with Alzheimer's disease. These pathways could be targeted with new or existing medicines to potentially help resensitize the brain to insulin and possibly slow down or even improve cognitive decline. This is the first study to directly demonstrate that insulin resistance occurs in the brains of people with Alzheimer's disease.
The deposition of amyloid beta in the brain of individuals with Alzheimer's disease is the focus of much research into both its cause and treatment. While there may not be a consensus as to whether the deposition contributes to the disease or is a consequence of the disease, there is agreement that it is not favoured thermodynamically, meaning that something else is promoting the process. Other proteins are often co-deposited in vivo with amyloid beta and one such protein is serum amyloid P component (or SAP). Recent evidence has suggested that SAP is elevated in Alzheimer's disease and a team of researchers from Keele University in Staffordshire, UK, led by Professor Chris Exley, has shown that physiologically-significant concentrations of SAP promote the deposition of amyloid beta under conditions approaching those found in vivo.