A study at Emory University School of Medicine has marked another step towards developing an effective blood test for Alzheimer’s disease. This study will be published in the August 28 issue of the journal, Neurology. William Hu, MD, PhD and assistant professor of Neurology at the university was the lead author of hits study; collaborators from University of Pennsylvania and Washington University, St. Louis, were also involved.

Six hundred participants from these institutions took part in the study; these participants were either healthy or diagnosed with Alzheimer’s disease (AD) or mild cognitive impairment (MCI). MCI can be a precursor to Alzheimer’s. The scientists measured the levels of 190 proteins in the blood of the participants. Results indicated that 17 proteins were present in significantly different levels in the blood of those with AD or MCI compared to the healthy volunteers. The researchers checked these 17 proteins with data from another 566 people in the multicenter Alzheimer’s Disease Neuroimaging Initiative. From this, they distinguished four proteins (apolipoprotein E, B-type natriuretic peptide, C-reactive protein, pancreatic polypeptide) that correlated with AD and MCI. In an analysis that clustered people into three groups (MCI, high risk of developing AD, and full AD), it was found that changes in blood levels of these foru proteins are linked to levels of beta-amyloid in the cerebrospinal fluid. Beta-amyloid is the protein that is believed to cause Alzheimer’s when accumulated in the brain.

While there is a way to go, these biomarkers give hope that a blood test for Alzheimer’s can be possible.

For the publication of the study, please visit http://www.ncbi.nlm.nih.gov/pubmed/22855860.

Source: http://scienceblog.com/56029/blood-test-for-alzheimers-gaining-ground/

Keywords: blood test; Alzheimer’s disease; beta-amyloid

Wendy Liu

August 13, 2012

Many clinical trials for Alzheimer's Drug failed recently.  Dimebon (Latrepirdine) is one of them.

The drug latrepirdine, known as Dimebon, has been featured in two studies previously published in the journal Molecular Psychiatry.The second study showed that latrepirdine could serve as treatment for Alzheimer’s disease, Parkinson’s, as well as other neurodegenerative conditions.

Led by researchers from Mount Sinai School of Medicine, the drug was tested in three different systems (yeast cells, mice cells, and mammal cells), and each system had an accumulation of alpha-synuclein, a protein that causes neurodegeneration. In all three systems, latrepirdine was able to trigger autophagy, a homeostatic process by which the cells break down their own components. The autophagy decreased the amount of synuclein that built up in the mice’s brains.

In the first study, the researchers found that the drug, by activating autophagy, was able to stop the accumulation of beta-amyloid in the brains of mice with Alzheimer’s disease, and their memories also improved. In addition, it was found that the yeast cells were protected by latrepirdine from the toxicity of alpha-synuclein.

Latrepirdine was approved by Russia in 1983 to be sold as an antihistamine in the country. After being effective in treating animal models with Alzheimer’s disease in the 1990s, it underwent a large Phase II clinical trial in Russia with results showing that it significantly improved cognitive function in Alzheimer’s patients with minimal side effects and was able to maintain that improvement. A Phase III clinical trial was carried out in the United States, but there was so sign of improvement in the Alzheimer’s patients.  Scientists now believe that the trial failed “because of a lack of understanding of how latrepirdine works”.

Currently, the researchers are seeing if the drug can help treat or prevent Parkinson’s disease, Lewy body dementia, etc, all of which are disorders related to high levels of alpha-synuclein.

Sources: http://www.medicalnewstoday.com/articles/248956.php


Keywords: drug; latrepiridine; alpha-synuclein; Alzheimer’s disease; Parkinson’s disease; research

Wendy Liu

August 14, 2012

A recent study suggests that consuming cocoa flavanols as part of a regulated diet could improve cognitive function. This study, conducted by researchers at the University of L’Aquila in L’Aquila, Italy, was published on August 14 in Hypertension.

Flavanols are a class of flavonoids (plant secondary metabolites with medicinal properties) that are abundant in teas, berries, apples, grapes, red wine, and chocolate. Flavanols can work as an antioxidant. This study involved 90 elderly participants with mild cognitive impairment (MCI), a condition that increases the risk of developing Alzheimer’s or some other form of dementia. The 90 patients were each randomized to consume a dairy-based cocoa flavanol drink of different amounts (990 milligrams, 520 milligrams, or 45 milligrams) for eight weeks. Their diet was cut off of other sources of flavanols. After eight weeks, they participated in neuropsychological tests, and results showed that those in the groups who drank higher levels of cocoa performed significantly higher in the tests than those who drank lower levels of cocoa. Those given the drinks with higher flavanol content also had decreased insulin resistance, blood pressure, and oxidative stress. The decreased insulin resistances levels contributed to 40 percent of the higher results in the cognitive tests.

However, the researchers acknowledge that this was just a small preliminary study that requires larger long-term studies before the results can be confirmed. They still need to determine the amount of cocoa flavanols needed to obtain the benefits and how long these benefits will last. While flavanols has the potential to help improve cognitive function as part of a healthy diet, it is discouraged that people should consume chocolate everyday because of this study.

Sources: http://www.healthcare-today.co.uk/news/cocoa-could-keep-dementia-at-bay/22509/


Keywords: cocoa; flavanols; mild cognitive impairment (MCI); research

Wendy Liu

August 14, 2012