Vitamin C treatment dissolves toxic Alzheimer’s proteins
Vitamin C could have a new role for treating Alzheimer's disease
Vitamin C might help patients with Alzheimer’s disease, shown recently in mouse studies. According to new findings, vitamin C treatment dissolves toxic proteins in the brain that are associated with Alzheimer’s disease, known as beta-amyloid plaques.
For the study, published in the Journal of Biological Chemistry, researchers from Lund University used vitamin C to treat brain tissue in mice suffering from Alzheimer’s disease.
Katrin Mani, reader in Molecular Medicine at Lund University said, "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.”
The role of vitamin C for treating a variety of diseases has been the subject of much research. The mouse study shows the vitamin might be useful for preventing and even treating Alzheimer’s disease.
Past studies have suggested high doses of vitamin E and vitamin C might prevent Alzheimer’s disease.
A 1998 observational study from M.C. Morris and colleagues at Rush Institute for Healthy Aging and Rush Alzheimer's Disease Center: “Vitamin E and vitamin C supplement use and risk of incident Alzheimer disease”, suggested vitamin C may reduce levels of oxidative stress and inflammation, thought to contribute to neurologic disease such as Alzheimer’s.
Mani says the vitamin is easily absorbed in high levels from juice and doesn’t have to come from fresh fruit.
"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.
Based on the study finding, the authors concluded low levels of vitamin C could play a role in onset of Alzheimer’s disease later in life in humans.
The Journal of Biological Chemistry
"Suppression of Amyloid β A11 Antibody Immunoreactivity by Vitamin C"
Fang Cheng et al.
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