Alzheimer’s and Vitamin E

Can vitamin E slow Alzheimer’s disease (AD) progression?

According to a new double-blind, placebo-controlled trial found that alpha tocopherol (2000IU/d vitamin E) reduced the rate of functional decline in 561 patients with mild to moderate AD.

In the vitamin E group, the delay in clinical progression of AD was translated to 19% per year compared with placebo or a delay of approximately 6.2 months over the follow-up period.

… do you include VitaminE rich foods in your diet? much love.

Reference:

Neurology Now (January 14, 2014)

Dysken, M.W. (2014). Journal of the American Medical Association.

 

liver disease drug may slow progression of parkinson’s disease

Sheffield Institute for Translational Neuroscience are hopeful that new research (published in Brain) may lead to a group of drugs that may slow the progression of Parkinson’s disease.

One of the major hypotheses for brain cell death in Parkinson’s is the malfunctioning of the mitochondria. The drug studied by the researchers at the Sheffield Institute includes compounds targeted to correct the faulty mitochondria, the power house of the cells of our body.

The synthetic drug identified by researchers, ‘Ursodeoxycholic acid‘ (UDCA), is a licensed drug has been used to treat liver disease. Researchers can now initiate clinical trials to verify the safety as well as the tolerability for Parkinson’s.

How exciting is this? Treatment options that will slow down or halt Parkinson’s progression – rather than just managing symptoms – have serious implications for improved quality of life! I’m looking forward to how the clinical trials progress! much love.

slowing Parkinson’s progression: a research update

alpha-synuclein is a protein encoded by the SNCA gene.

Although we are still not certain of what it does, we do know it makes up Lewy Bodies, clusters of proteins that are a pathological hallmark of Parkinson’s disease and other dementias (lewy body dementias). It is thought that in Parkinson’s disease, the variability in alpha-synuclein gene produces either too much alpha-synuclein protein or causes it to malfunction — which may be toxic to brain cells and to result in neuron dysfunction.

Some of the ways in which research is targeting alpha-synuclein is by:

  • a vaccine that binds to alpha-synuclein and clears it from the brain
  • compounds to stop alpha-synuclein from clumping (avoiding lewy body formation)
  • compound to break up alpha-synuclein clumps (breaking up formation of lewy bodies)

Recent research developments include a chemical compound that slows down the onset and progression of Parkinson’s disease in mice. Griese and Griesinger in Gottingen have developed a substance which, in mouse models of the disease, reduces the rate of growth of the alpha-synuclein deposits and delays nerve cell degeneration. As a consequence, mice treated with this agent remain disease-free for longer than non-medicated controls. The current gold-standard, Levodopa, controls Parkinson’s symptoms by enhancing the function of the surviving nerve cells in the substantia nigra. This compound shows promise in slowing down the progression, according to their lab results; the earlier the onset of treatment, the longer the animals remained disease free.

(Max-Planck-Gesellschaft (2013, April 22). Putting the brakes on Parkinson’s.ScienceDaily. Retrieved May 12, 2013, from http://www.sciencedaily.com­/releases/2013/04/130422111147.htm#.UXa4E78jkGQ)

Another research effort looking to halt Parkinson’s disease progression involves GM1 glanglioside. GM1 impacts neuron plasticity, repair mechanisms, and neurotrophin release.

A study published in November 2012 showed that GM1 ganglioside improved symptoms and slowed disease progression during a two and a half-year trial in persons with Parkinson’s. Dr. Jefferson, published in the Journal of the Neurological Sciences, followed 77 subjects over a 120-week period and 17 control subjects as comparison.  GM1 group had significant improvement in UPDRS motor scores and maintained much of the initial benefit of GM1 treatment, (i.e. showed relatively minor symptom progression compared to patients using standard anti-Parkinson medications).

(Jay S. Schneider, Stephen M. Gollomp, Stephanie Sendek, Amy Colcher, Franca Cambi, Wei Du. A randomized, controlled, delayed start trial of GM1 ganglioside in treated Parkinson’s disease patients. Journal of the Neurological Sciences, 2012; DOI:10.1016/j.jns.2012.10.024)

… some very interesting drug developments on the horizon. it’s a long process from developing compounds, animal testing, clinical testing etc. … but nice to know there are possibilities on the horizon! much love