"Good" Cholesterol and the MS Brain

New research, presented at the annual meeting of the Society of Neuroscience, finds a link to the level of a cholesterol transport protein and MS disease severity.  This research provides us another link to blood and the cardiovascular system, which I'll get into at the end of this note. 

First, let's review the announcement.
http://www.medscape.com/viewarticle/814798

ApoA1 is the main structural protein found in HDL, or what we call "good" cholesterol, and it is found to be low in pwMS.
Blood levels of the reverse cholesterol transport protein apolipoprotein A1 (ApoA1) are low in patients with multiple sclerosis (MS) and correlate with disease severity, new research shows.

ApoA1 is the most abundant component of high-density lipoprotein cholesterol and is known to protect against inflammation.

Dr. Gardner and colleagues investigated ApoA1 levels in 53 patients with relapsing-remitting MS, 50 with secondary progressive MS, 53 with primary progressive MS, and 57 healthy controls. "Remarkably, all MS patients had less ApoA1 than controls," they report in a meeting abstract.

ApoA1 was reduced by approximately 25% in patients with relapsing-remitting MS, 50% in those with secondary progressive MS, and 75% in patients with primary progressive MS, the most severe form of the disease.

I'm always alarmed when neurologists claim a finding like this is "surprising"--especially since lower levels of ApoA1 have been found in other diseases of neurodegeneration.

In Alzheimer's, the connection of more severe AD with low levels of ApoA1 has been established.  Higher levels of ApoA1 are related to sharper mental abilities and memory. 

Low levels of ApoA1 are correlated with more severe Alzheimer's Disease, and high levels of ApoA1 with a lower risk of AD --see Merched et al., 2000; Saczynski et al., 2007; Bates et al., 2009 

Other studies have hinted at a cognitive effect. High HDL levels associate with sharper mental abilities in the elderly (see ARF related news story on Barzilai et al., 2006), while low HDL levels are a risk factor for memory decline in middle-aged adults (see Singh-Manoux et al., 2008). What might be behind these apparent benefits? ApoA1 is known to have anti-inflammatory effects, and indeed, in a mouse model of brain inflammation, an ApoA1 mimetic improved cognitive deficits (see Buga et al., 2006). http://www.alzforum.org/new/detail.asp?id=2574

In Parkinson's, the connection of ApoA1 as a biomarker for disease risk has been established.  Lower levels of ApoA1 correlated with earlier onset of Parkinson's Disease while higher levels of ApoA1 were shown to be protective.

One of the best candidate protein biomarkers to emerge from discovery screening was apolipoprotein A1 (ApoA1; p = 0.001). Low levels of ApoA1 correlated with earlier PD onset, with a 26% decrease in risk of developing PD associated with each tertile increase in ApoA1 (Cox proportional hazards, p < 0.001, hazard ratio = 0.742). The association between plasma ApoA1 levels and age at PD onset was replicated in an independent cohort of PD patients (p < 0.001). Finally, in the PARS cohort of high-risk, asymptomatic subjects, lower plasma levels of ApoA1 were associated with greater putaminal DAT deficit (p = 0.037).

Lower ApoA1 levels correlate with dopaminergic system vulnerability in symptomatic PD patients and in asymptomatic individuals with physiological reductions in dopamine transporter density consistent with prodromal PD. Plasma ApoA1 may be a new biomarker for PD risk.

http://www.ncbi.nlm.nih.gov/pubmed/23447138

What does this all mean?  

It means ApoA1 levels are not just important for pwMS, they are important to monitor in all neurodegenerative disease.  It means the heart and brain are connected by our blood flow.  It means you can protect your brain by raising your HDL numbers.

I believe it's important to look at all diseases of neurodegeneration and consider blood flow and serum markers.

This also means that we have to look at the connection between our lives, our hearts and our brain health.  How can we increase our HDL, or good cholesterol--and thereby protect our brains from inflammation and further damage?  While labs work on ways to make drugs to raise our good cholesterol, we can consider how to do this ourselves.

How to raise HDL--or good cholesterol and help your brain.

LIFESTYLE is the most important means to increase HDL.

1. Don't smoke.  Quitting smoking will increase good cholesterol by 10%

2. Lose weight.  Extra weight depletes HDL.

3. Exercise.  Within 2 months of regular exercise, you can increase your HDL by 5%

4. Choose healthier fats for your diet. Avoid transfats, choose omega 3s and monosaturated fats found in nuts, olive oil, and fish

5. Add fiber to your diet--lots of fresh fruits and vegetables, legumes and oats

6. Limit alcohol consumption.

http://www.mayoclinic.com/health/hdl-cholesterol/CL00030/NSECTIONGROUP=2

7. Check your vitamin D, magnesium, calcium and zinc levels--make sure they are in balance.
http://www.ncbi.nlm.nih.gov/pubmed/7608827

Hope this information helps your heart and helps your brain.
Because they are connected,
Joan

Blocked blood vessels:  New research from Rush University

September 1, 2011 at 1:28pm

Dr. Aron Buchman is a neurologist at Rush University in Chicago.  For the past 20 years, he has been studying the aging brain and subtle changes that preceed Alzheimer's and Parkinson's diagnoses.  Here is the press regarding his most recent study, which looks at the brains after the participants have passed---

http://www.eurekalert.org/pub_releases/2011-09/rumc-soa082911.php

Signs of aging may be linked to undetected blocked brain blood vessels

Many common signs of aging, such as shaking hands, stooped posture and walking slower, may be due to tiny blocked vessels in the brain that can't be detected by current technology.

In a study reported in Stroke: Journal of the American Heart Association, researchers from Rush University Medical Center, Chicago, examined brain autopsies of older people and found:

Microscopic lesions or infarcts — too small to be detected using brain imaging — were in 30 percent of the brains of people who had no diagnosed brain disease or stroke.

Those who had the most trouble walking had multiple brain lesions. Two-thirds of the people had at least one blood vessel abnormality, suggesting a possible link between the blocked vessels and the familiar signs of aging.

"This is very surprising," said Dr. Aron S. Buchman, lead author of the study and associate professor of neurological sciences at Rush. "The public health implications are significant because we are not identifying the 30 percent who have undiagnosed small vessel disease that is not picked up by current technology. We need additional tools in order to identify this population."

Vitamin D provides "Vasculoprotection"

July 13, 2010 at 10:06am

We all know about the link of low levels of vitamin D associated with MS progression.  The common wisdom is that this is because vit. D modulates the immune system. But now there are more and more studies coming forward showing linkage in other neurological disorders and general brain health via the vasculature.  

Vitamin D supplementation can protects vasculature of the brain.  

Low vitamin D levels are linked to brain atrophy.

From Scientific American:

Low vitamin D in Parkinsons and Dementia--

"The first study, led by Paul Knekt and colleagues at the National Institute for Health and Welfare, Finland, examined levels of vitamin D in the blood of 3,173 Finnish men and women aged 50-79 determined to be free of Parkinson's disease at the start of the study. The researchers then examined the incidence of Parkinson's disease in these participants over a 29-year follow-up period. They found that participants with the highest levels of vitamin D (more than 50 nmol/L) had a 65 percent lower risk of developing Parkinson's disease than those with the lowest vitamin D levels (less than 25 nmol/L).

In the second study, David Llewellyn of the University of Exeter and colleagues examined vitamin D levels among 858 Italian men and women age 65 and older. They found that more than half of the participants with dementia were vitamin D deficient .

___________________________________________________________

And here is news of a study at SUNY Buffalo, from earlier this spring:

"Low vitamin D levels may be associated with more advanced physical disability and cognitive impairment in persons with multiple sclerosis, studies conducted by neurologists at the University at Buffalo have shown.

http://www.sciencedaily.com/releases/2010/04/100429153955.htm

Their results, reported at the American Academy of Neurology meeting, held earlier this month, indicated that:

The majority of MS patients and healthy controls had insufficient vitamin D levels.

Clinical evaluation and magnetic resonance imaging (MRI) images show low blood levels of total vitamin D and certain active vitamin D byproducts are associated with increased disability, brain atrophy and brain lesion load in MS patients.

A potential association exists between cognitive impairment in MS patients and low vitamin D levels."

__________________________________________________________

Now, how could this situation be compounded when we consider CCSVI as a factor in developing MS? I believe it's all about protecting the brain from further vascular damage. Here's a wonderful research paper on how Vitamin D can provide "vasculoprotection" of the brain.

http://ddr.nal.usda.gov/bitstream/10113/27508/1/IND44182071.pdf

"Vitamin D may help to protect against cognitive deterioration and dementia, specifically, vascular dementia and Alzheimer’s disease, through vasculoprotection (Lind et al., 1987; Burgess et al., 1990; O’Connell et al., 1997; Pfeifer et al., 2001; Wang et al., 2001; Zittermann et al., 2003; Wang et al., 2008a,b), preservation of neurons (Sutherland et al., 1992; Landfield and Cadwallader-Neal, 1998; Brewer et al., 2001), and protection against risk factors for cognitive dysfunction (Lind et al., 1987; Burgess et al., 1990; Hypponen et al., 2001; Pfeifer et al., 2001; Li et al., 2002, 2004; Zittermann et al., 2003; Bisc- hoff-Ferrari et al., 2004; Wang et al., 2008a,b).

We did observe an inverse association between 25(OH) D concentration and presence of white matter hyperintensities and large vessel infarcts; indicators of cerebrovascular disease (Buell et al, in preparation). Consistent with this finding, we observed a positive association between vitamin D concentrations and the integrity and structural arrangement of white matter fibers using diffuser tensor imaging. Further studies designed to provide information on the temporal relationship of 25(OH)D and brain morphology are warranted.

420 J.S. Buell, B. Dawson-Hughes / Molecular Aspects of Medicine 29 (2008) 415–422"

The underlying message is, get adequate vitamin D and sunshine. You're helping your brain, and may be slowing or preventing atrophy.

Joan