How exercise improves brain health

Last week I mentioned some specific exercises targeted to PD symptoms (see HERE and HERE)… today I want to share WHY exercise is so important for brain health.

New Research out of the Dana-Faber Cancer institute and Harvard Medical School (Spiegelman & Greenberg, Cell Metabolism 2013) shows that endurance exercise, such as distance running or cycling, releases a protein (FNDC5) that improves brain health while promoting the growth of nerves associated with cognition.

Alzheimers and Exercise

In laboratory rats, PGC-1α (which is also found in humans) led to improvements in protein FNDC5 and Brain Derived Neurotrophic Factors (BDNF). PGC-1α is thought to coordinate the gene response to exercise,  blood pressure and development of obesity.

Exercise stimulates BDNF expression in the hippocampus, the part of the human brain associated with memory and learning. In this study, specific improvements in awareness and memory recall was demonstrated. BDNFs are also responsible for creating new brain connections (neurons, synapses)

Memory is Enhanced by Exercise

Rich Exercise Regimens Promote Cognitive Health

So, keep moving! much love.

Other reference:

http://www.ibtimes.com/exercise-improves-brain-health-could-lead-new-alzheimers-parkinsons-treatments-1424338#.Ul35Vb9PDvQ.twitter

images from bodbot.com

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Whole, Rethinking nutrition : summer reads

Dr. Campbell, in the follow up to his book, The China Study, discusses the implications of a Whole Food Plant Based (WFPB) diet to research, social policy and healthcare. The China Study was a cross-sectional ecological design that found that higher consumption of animal products in different regions of China was correlated to greater the incidence of and mortality from cancer, heart disease, stroke etc.

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His central thesis is around the contribution of poor nutrition (nutritional imbalance) to cancer occurrence, or disease occurrence in general. Specifically, he states that a high protein diet increases MFO enzyme activity, leading to increased binding of toxic metabolite (AF) to DNA, causing more cancer.

He empowers us to have control over our health through the simple act of choosing what we eat. Dr Campbell states the current medical system focuses exclusively on treating symptoms, and steadfastly ignoring the root causes.  He believes the power of WFPB diet to act harmoniously on a broad variety of illnesses and that poor nutrition causes more disease than the “disease-care” system currently acknowledges.

He emphasizes that whole foods are astoundingly more potent as the same amount of isolated vitamins and supplement. This is because compounds in foods work together to be more effect in context of the whole than when in an isolated pill. As such, we don’t necessarily know how much of these vitamins and minerals we are getting from the food we eat… but that doesn’t matter because the body is smart enough to take what it needs from the foods we eat (even plant-based protein!) and waste the rest! How smart ?!

whole-nutrition-campbell

… some food for thought! much love.

prions & other misfolded proteins : summer reads

A prion is thought of as a protein molecule with no genetic material that can infect, multiply and kill. Prions are caused by misfolded ‘normal’ proteins and were “discovered” by Stanley Prusiner (who won a nobel prize).

I recently read Fatal Flaw by Jay Ingram (of Daily Planet and Quirks & Quacks), “the rough and tumble story of prions, filled with rivals, eccentrics, meddlesome governments and brilliant creatives“.

fatal_flaw_book_jay_ingram

As I sat down with my coffee and danish, I started to read about cannibalism in New Guinea and a disease “Kuru”. How appetizing. This book tracks prion disease from kuru (thought to be caused by cannibalism of prion-diseased brains), scrapie in sheep (spongiform encephalopathy), related to bovine spongiform encephalopathy (mad cow disease), chronic wasting disease in North American deer, and finally to Creutzfeldt-Jakob disease.

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The book eventually discusses other diseases that, while not infectious, do involve misfolded proteins; including amyotrophic lateral sclerosis (Lou Gehrig’s), Parkinson’s disease, chronic traumatic encephalopathy (“punch drunk”) and Alzheimer’s disease.

How better understanding prion disease relates to Parkinson’s disease is in the misfolded alpha-synuclein protein deposits that clump together to form lewy bodies. These invading misfolded proteins have a long incubation period (similar to prion disease), where it can be anywhere from 5-30 years before Parkinson’s symptoms even develop. Lewy bodies first accumulate in the nerves of the gut, travel in the spinal cord before spreading to the lower brain (substantia nigra = when symptoms develop) and eventually to cerebral cortex (which may cause dementia). This migration is thought to support the environmental theory of Parkinson’s and paralleled how cow’s who developed Mad Cow Disease ate infected meat and bone meal, which travelled from their stomach to their brain.

aggregating_prions

Investigation into prions will help Parkinson’s by understanding

1) how midfolded proteins have the ability to move from one cell to another

2) long disease incubation periods

3) possibilities of stabilize proteins to make them resistent to midfolding, which may halt/reverse disease progression.

if you can get past the cannibalism and infected animals (sheep, cows, deer), it really tells the story of how science begins to understand disease, proteins, DNA, outbreaks, and neurodegenerative conditions. 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

Paleo for Parkinson’s?

So, Darc and I decided to do a cleanse for the month of March. Spring is a great time to detox… your body and your living space (we moved apartments, so we also did some major spring cleaning of our ‘stuff’!). We decided to follow Tim Ferris’ 4-hour body Slow Carb Diet … basically cutting out everything but protein and veggies. It was hard, at first… then after a month we decided to extend it a bit longer. Now, a low carb diet is becoming a habit (are you surprise? this is from the guy who bakes … and I mean CHECK OUT THESE pancakes, english muffins, bread, cinnamon buns, pizza, AND croissants!!).

Lately, we’ve been looking into the Paleo diet (…though being a vegetarian i’m a bit unsure of where I’m going to get all my protein without legumes) and we came across this great book at the library…

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… and whatdya know, they have a section on eating for Neurological health, including Parkinson’s disease!

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The book suggests some nutrients, such as B vitamins, Vitamin C, D & E, magnesium,  potassium, omega-3’s, probiotics, zinc among others…

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It also discusses dietary / lifestyle factors you should add (fats, antioxidants, massage, stress-management) and avoid (gluten, dairy, sweeteners, caffeine) … though I DO NOT agree with avoiding high-intensity exercise, as research demonstrates it IS beneficial.
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… and finally some considerations around protein, Vitamin B6 and Levodopa.

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… now I’m curious… Let me know IN THE COMMENTS BELOWdo YOU follow ay special diet plans?

Have you tried a gluten-free or Paleo diet?

How does diet modification change YOUR Parkinson’s management (because we all know everyone is different!)??

much love.

from research to real life – curcumin attacks proteins related to Parkinson’s disease


Curcumin
is a natural compound in the Indian spice, Turmeric, part of the ginger family.

The main idea: In Parkinson’s disease, abnormal clumping of the protein alpha-synuclein occurs. New research shows curcumin may bind to the alpha-synuclein proteins and prevent the abnormal folding and clumping that may be the first steps to Parkinson’s disease.

Research: Curcumin prevents aggregation in α-synuclein by increasing reconfiguration rate

Real life: Curcumin shows promise in attacking Parkinson’s disease

chick pea curry with turmeric

However, turmeric doesn’t go directly to the brain where this clumping occurs, so don’t go out and fill up on curry’s just yet (or do, it’s pretty delicious!). much love.

from research to real life – calcium may advance Parkinson’s disease

I’m starting a new regular post… from research to real life. There’s so much information out there, it’s hard to keep track of it all! I will present new (and exciting!) research in both a scientific and news media format, so the ideas come across in whatever way you choose to get your information!

I thought this was an interesting article on calcium and dopaminergic neurons.

The main idea: calcium stresses dopamine neurons, leading to premature aging and cell death. There is ongoing research into drugs that shut down Cav1.3 (a membrane protein that controls calcium release) to relieve stress on dopamine cells… and may slow disease progression.

ResearchCaV1.3-selective L-type calcium channel antagonists as potential new therapeutics for Parkinson’s disease

Real lifeParkinson’s breakthough could slow disease progression – Dementia News – –.

enjoy! much love.