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Posts Tagged ‘aging’

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The above images are eigenfaces … which are statistically distilled basic components of human faces … from which ANY human face can be reconstructed as a combination of the above basic components.  It’s a great mathematical trick – particularly if you’re into the whole mass surveillance and electronic police state thing.

If you are more into the whole, helping people and medical care thing, check out the global consortia at ENIGMA who have been carrying out massive genetic and brain scanning studies – like this one involving 437,607 SNPs in 31,622 voxels in 731 subjects using their new method, vGeneWAS, to study Alzheimer’s Disease:

“We hypothesized that vGeneWAS would, in some situations, have greater power to detect associations than existing SNP-based methods. One such situation might be when a gene contains many loci with weak individual effects. In addition, we expected that vGeneWAS would have greater overall power than mass SNP-based methods, like vGWAS, because of the drastic reduction in the effective number of statistical tests performed.”

The vGeneWAS method relies on the calculation of “eigenSNPs” which are eigenvectors that describe a matrix of n subjects by m SNPs in an individual gene (an n-x-m matrix of 1’s,0’s,-1’s for aa, aA, AA genotypes).  EigenSNPs are sort of like eigenfaces insofar as eigenSNPs (which are not actual SNPs) capture the majority of variance, or the basic essence of an individual gene … but seriously, you should read the original article ’cause every stats test I ever took totally punched me in the face.

In any case, the eigenSNP-by-voxel method pulled out some legit results such as rs2373115 (where the G-allele confers risk) in the GAB2 gene  which has repeatedly been implicated in the risk of age-related late-onset Alzheimer’s Disease (in folks who carry ApoE4  rs429358(C) alleles).  The authors found that the genetic risk of AD conferred by GAB2 may arise by way of GAB2’s effect on brain structure in the periventricular areas, which have been known to be among the first brain regions to show AD-related changes (time-lapse movie of AD tissue loss in the brain).

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Mitochondrial damage is associated with premature aging in the body and related disorders such as Parkinson’s Disease in the brain.  If you want to grow old and healthy … be nice to your mitochondria … eat healthy foods and exercise.

When mitochondria are damaged, cells can use proteolysis to clean them out, but when this cleaning out process fails … trouble ensues.   PINK1 plays a role on the clearance of damaged mitochondria as revealed by Dr. Derek P. Narendra and colleagues: PINK1 Is Selectively Stabilized on Impaired Mitochondria to Activate Parkin

Since neurons in the Substantia Nigra are postmitotic, any mitochondrial damage they acquire could accumulate over an organism’s lifetime, leading to progressive mitochondrial dysfunction—including increased oxidative stress, decreased calcium buffering capacity, loss of ATP, and, eventually, cell death—unless quality control processes eliminate the damaged mitochondria.

The findings we report in this paper suggest a new model in which PINK1 and Parkin together sense mitochondria in distress and selectively target them for degradation. In this pathway, PINK1 acts as a flag that accumulates on dysfunctional mitochondria and then signals to Parkin, which tags these mitochondria for destruction. Since disease-causing mutations in PINK1 or Parkin disrupt this pathway, patients with these mutations may not be able to clean up their damaged mitochondria, leading to the neuronal damage typical of parkinsonism.

Dr. Terry Wahls has some very inspiring experiences to share on the topic of mitochondrial care.

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Wobble base pair guanine uracil (GU)

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Hands shake and wobble as the decades pass … moreso in some.

A recently evolved “T” allele (rs12720208) in the  3′ untranslated region (3′ UTR) of the FGF20 gene has been implicated in the risk of Parkinson’s Disease … namely by creating a wobbly G:U base-pair between microRNA-433 (miR-433) and the FGF20 transcript.  Since the normal function of microRNA-433 is to repress translation of proteins (such as FGF20), it is suspected that the PD risk “T” allele carriers make relatively more FGF20 … which, in turn … leads to the production of higher levels of alpha-synuclein (the main component of Lewy body fibrils, a pathological marker of diseases such as PD).  This newly evolved T-allele has also been associated with brain structural differences in healthy individuals.

My hands will shake and wobble as the decades pass … but not because I carry the G:U wobble pairing between miR-433:FGF20.  My 23andMe profile shows that I carry 2 C alleles and will produce the thermodynamically favorable G:C pairing.  Something to keep in mind as I lose my mind in the decades to come.

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… from The Big Picture

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Have you ever suddenly realized, “OMG, I’m just like my dad (or mom)!”  Oh, the horror .. the horror.  Here’s John Updike from A Month of Sundays:

Also my father, who in space-time occupied a stark room of a rest home an hour distant, which he furnished with a vigorous and Protean suite of senility’s phantoms, was in a genetic dimension unfolding within me, as time advanced, and occupying my body like, as Colette had written to illustrate another phenomenon, a hand being forced into a tight glove.

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Telomere caps he:תמונה:Telomere caps.gif
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A startling article that appears today in the science journal Nature, shows that reactivation and restoration of DNA telomeres was sufficient to reverse the aging process! From the article:

Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice.

Accumulating evidence implicating telomere damage as a driver of age-associated organ decline and disease risk1, 3 and the marked reversal of systemic degenerative phenotypes in adult mice observed here support the development of regenerative strategies designed to restore telomere integrity.

Love yourself, love your DNA – especially the telomeres ! For more on this topic, see a few weeks back, when I covered a research article by Nobel Prize winning scientist Elizabeth Blackburn on meditation, telomeres and longevity.

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Stick model of NAD + , based on x-ray diffract...
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Yogis are by far the healthiest eaters I have ever met.  If you’re reading this blog, you’re probably one of them – faithful in the observance of your Yamas and Niyamas – leaving me  reluctant to confess my own (pre-yoga) pizza-scarfing, soda-swilling ways.  Please don’t hold it against me.  I’ve changed, really.

Here – as plain as I can make it – is the scientific reason why eating a low-calorie vegetarian diet is a good thing.  Good, as in living longer and cancer-free.

All you need to know is that when you eat less, your levels of Nicotinamide adenine dinucleotide (NAD – the contorted, yogic-looking molecule shown at left) are HIGH – and this increases the activity of the “longevity gene” SIR2. The amazing life-extending effects of the NAD-dependent SIR2 genes are described in detail on Leonard Guarente’s website at M.I.T.:

The discovery that Sir2p requires NAD for its activity immediately suggested a link between SIR2 activity and caloric restriction. This link was strengthened by the observation that life span extension by caloric restriction requires Sir2 protein. Caloric restriction is likely to reduce the carbon flow through glycolysis and result in more free cytoplasmic NAD. SIR2 could act as a sensor of NAD levels within the nucleus. Under conditions of caloric restriction, NAD levels are high, SIR2 is activated, and the rate of aging is decreased.

The hard science link between cancer and NAD is more recent – this week in fact – with the release of a study entitled, “Transcriptional regulation of BRCA1 expression by a metabolic switch” [doi:10.1038/nsmb.1941].  Here the researchers found that NAD/NADH levels via binding to CTBP1 can regulate the anti-tumor properties of BRCA1.  In a nutshell, a high-calorie diet leads to LOW levels of NAD which has the net effect (via CTBP1) of turning OFF the anti-tumor gene BRCA1 (a bad thing).  From the article:

The elevated expression of estrogen in the context of higher levels of NADH or lower NAD+/NADH ratios due to high caloric intake and/or obesity could establish a state in which the pro-proliferative effects of estrogen are not completely balanced by the protective functions of BRCA1 that would normally restrain estrogen-induced proliferation and heighten genome surveillance.

I realize that most yoga folks need no such hard science to convince them of the merits of a low-calorie, healthy diet.  In the science-world however, empirical evidence can take decades to gather, so its an important milestone to now have established causal links between caloric intake, longevity and cancer risk.

For (former) junk food junkies like myself, there is no room to debate or side-step the issue.  Eat less, eat healthy – live longer and cancer-free.  More on yoga and aging (here, here, here).  Now, off to the shala for NADasana pose!

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