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Tuesday, August 23, 2011

Treatment With Vitamin C Dissolves Toxic Protein Aggregates in Alzheimer's Disease

Treatment With Vitamin C Dissolves Toxic Protein Aggregates in Alzheimer's Disease, but could it work for bvFTD (Frontotemporal Degeneration) also? Ummmmm ...maybe!

It would be a pleasant addition to any diet.
There have been so many outrageous claims made over the years about the benefits of vitamin C that I am very skeptical. It does seem that almost any antioxidant is beneficial in treating tauopathies. Of course, one cannot soak a living brain in orange juice, so a little more research needs to be done on how much, how long, and what forms can be absorbed by humans.

ScienceDaily (Aug. 18, 2011) — Researchers at Lund University have discovered a new function for vitamin C. Treatment with vitamin C can dissolve the toxic protein aggregates that build up in the brain in Alzheimer's disease.
The research findings are now being presented in the Journal of Biological Chemistry.

The brains of people with Alzheimer's disease contain lumps of so-called amyloid plaques which consist of misfolded protein aggregates. They cause nerve cell death in the brain and the first nerves to be attacked are the ones in the brain's memory centre.

"When we treated brain tissue from mice suffering from Alzheimer's disease with vitamin C, we could see that the toxic protein aggregates were dissolved. Our results show a previously unknown model for how vitamin C affects the amyloid plaques," says Katrin Mani, reader in Molecular Medicine at Lund University.

"Another interesting finding is that the useful vitamin C does not need to come from fresh fruit. In our experiments, we show that the vitamin C can also be absorbed in larger quantities in the form of dehydroascorbic acid from juice that has been kept overnight in a refrigerator, for example."

There is at present no treatment that cures Alzheimer's disease, but the research is aimed at treatments and methods to delay and alleviate the progression of the disease by addressing the symptoms.

That antioxidants such as vitamin C have a protective effect against a number of diseases, from the common cold to heart attacks and dementia, has long been a current focus of research.

"The notion that vitamin C can have a positive effect on Alzheimer's disease is controversial, but our results open up new opportunities for research into Alzheimer's and the possibilities offered by vitamin C," says Katrin Mani.

Comments are welcome.

Any Drug Which Controls Brain Cell Death Will Probably Have Potential To Treat FTD

Alzheimer's Disease Drug Treats Traumatic Brain Injury

ScienceDaily (July 14, 2009) — The destructive cellular pathways activated in Alzheimer's disease are also triggered following traumatic brain injury, say researchers from Georgetown University Medical Center (GUMC). They say this finding suggests that novel therapy might successfully target both conditions.

In an oral presentation at the Alzheimer's Association 2009 International Conference on Alzheimer's Disease, the scientists will show that deactivating these pathways in part by using a gamma secretase inhibitor - a class of Alzheimer's disease drugs currently being tested - reduced loss of neurons in animal models of traumatic brain injury and protected the animals against motor and cognitive deficits.

"The goal for both diseases is to prevent neuronal cell death, and this study suggests that one therapy could possibly work for both," says the study's lead author, neuroscientist Mark Burns, PhD, an assistant professor at GUMC.

Both disorders are associated with build-up of beta amyloid, a toxic brain peptide. This substance is commonly found in the brains of elderly patients who died from Alzheimer's disease, but has also been found in a third of traumatic brain injury victims, some of whom are children, Burns says. It is also known that people who experience such a brain injury have a 400 percent increased risk of developing Alzheimer's disease.

Burns says that buildup of beta amyloid occurs in a second wave of damage that follows immediate "necrotic" death of nerve cells after traumatic brain injury. This secondary injury can last months, if not years, resulting in large holes within brain tissue.

Amyloid peptides are produced when a long brain protein known as the amyloid precursor protein (APP) is cut in two by the enzyme beta secretase, and then cut once again by a second enzyme known as gamma secretase. Agents that inhibit the activity of gamma secretase are now being studied as treatment for Alzheimer's disease.

In this study, researchers used mice that were either treated with DAPT, an experimental gamma secretase inhibitor, or mice which were "BACE knock-outs" – so called because they were genetically altered in such a way that they could not produce beta secretase. In unaltered and untreated "normal" mice, brain injury resulted in a rapid accumulation of beta amyloid, along with cognitive and motor deficits. But DAPT and BACE knock-out mice had brain lesions that were as much as 70 percent smaller than control animals and they experienced minimal impairment.

The findings further cement the connection between Alzheimer's disease and traumatic brain injury, Burns says, and show that "modulation of beta and gamma secretase may provide novel therapeutic targets for the treatment of traumatic brain injury."

The study was funded by grants from the National Institutes of Health and by the Klingel Family Foundation. The scientists report no potential financial conflicts in this research. Georgetown University has filed a patent application for the technology involved in this research.