Shilajit Boosts CoQ10 EfficiencyFebruary 2016
By Jonathan Stoddard
Coenzyme Q10 (CoQ10) fuels cellular energy by boosting mitochondrial function.1-3
As we age, our internal production of CoQ10 declines and we face an energy crisis.
When cells are deficient in CoQ10, the result is accelerated aging.1,4 Studies have shown that CoQ10 can help protect against a host of degenerative illnesses.5-9
Ever since CoQ10 was discovered in 1957, scientists have strived to find ways to make it work more efficiently in the body.
A major advance occurred when Life Extension® introduced the ubiquinol form of CoQ10 in 2006. Compared to the previous version, ubiquinol better absorbs into the bloodstream and markedly slows aging in the animal model.
As if this weren’t enough, researchers have shown that a nutrient-rich biomass called shilajit can boost CoQ10 efficiency.10 Found in the Himalayas, shilajit is prized for its ability to carry energy and nutrition into the body.11
When CoQ10 and shilajit are combined, scientists have discovered improved mitochondrial function, enhancement of the mitochondria’s ability to convert food into energy, and increased energy available to tissues.10,12
The combination of CoQ10 and shilajit has been shown to result in elevated levels of the body’s primary source of energy: ATP (adenosine triphosphate).10,12
Shilajit plus CoQ10 enhances mitochondrial health, which is a vital factor in preventing aging and disease at the cellular level.
Ancient Remedy Solves Modern Energy Crisis
For centuries, practitioners of Ayurvedic medicine (one of the world’s oldest holistic healing systems) relied on a curious substance called shilajit to treat or prevent a host of health problems.13-16 Preserved in the rocks of the Himalayas, shilajit is a rich organic material that forms in the part of the earth called the rhizosphere—the thin layer where living roots and microorganisms interact with the rocky core of the planet itself.13
In traditional medicine, shilajit is prized for its ability to restore energy, increase fertility, enhance immunity, and safeguard memory against the effects of aging.10,12
Now, modern scientists have proven that this rare herbal tonic beneficially impacts cellular energy, diabetes, Alzheimer’s, and Parkinson’s disease, and that it can reduce inflammation, improve memory, protect against cognitive decline, and more.10,12,13,17,18
As scientists further investigated the properties of shilajit, they determined that it is an adaptogen,13,14 which is a substance that helps the body adapt to internal and external stressors. In other words, shilajit is a natural stress-fighting, fatigue-busting substance that can not only help one feel revitalized, but can help rejuvenate tired cells. This can beneficially impact the entire body.
So how does it work?
It’s simple. Shilajit restores and sustains cellular energy by enhancing the production of the body’s primary source of energy: adenosine triphosphate, or simply ATP.12 ATP is the usable energy that is formed when organelles called mitochondria convert energy from food. As people age, this conversion process becomes sluggish, resulting in a body-wide energy deficiency.
Mitochondria and Aging
It would be impossible to overstate the importance mitochondria play in overall health and longevity. Mitochondria are cellular generators responsible for producing the body’s primary source of energy, called adenosine triphosphate (ATP). ATP provides at least 95% of the cellular energy that powers all living functions, from muscle contractions to hormone production, and everything in between.
Unfortunately, mitochondria function less and less efficiently as we age, causing a ripple effect of health consequences throughout the entire body. Less available energy means organs and tissues function less efficiently. This makes mitochondrial dysfunction especially damaging for the heart and brain, since they have the highest energy demands in the body.19
It should come as no surprise, then, that mitochondrial dysfunction has been linked to numerous degenerative illnesses, ranging from diabetes to neurological disorders to heart failure.20,21
The high energy output of mitochondria makes them highly vulnerable to oxidative damage.22-26 Evidence strongly indicates that over time, accumulated damage to the DNA of the mitochondria leads directly to metabolic disorders (such as diabetes) and degenerative disorders (such as Alzheimer’s).27-36
Ultimately, the downstream effects caused by mitochondrial dysfunction speed aging and death. The scientific evidence on this point is so strong that a growing number of cell biologists believe that the number and functionality of the mitochondria can specifically determine an individual’s longevity.37-39
The good news is that it’s not only possible to slow this cellular aging process but reverse it. The key lies in a nutrient you’re already familiar with: coenzyme Q10.
CoQ10 and Mitochondria
CoQ10 is already well-known for its ability to protect cells from damage, and for its remarkable effects against common heart ailments and neurological disorders.
What you might not know is that CoQ10 is absolutely essential for normal mitochondrial function (namely, the production and transfer of energy).1-3
Studies have found that when cells or organisms are deficient in CoQ10, it results in increased mitochondrial oxidative stress and accelerated aging.1,4 Supplementation with the right form of CoQ10 has been shown to slow aging in the animal model and extend life span.5,6
One study showed that rats supplemented with CoQ10 experience an 11.7% increase in average life span.40 In human terms, based on today’s life expectancy of 78.8 years, this translates to a more than nine-year increase in life span.41
The surge of available energy made possible by CoQ10 is especially beneficial for the heart. Studies have found that CoQ10 supplementation improves cardiac systolic function and ejection fraction.42,43 Another study showed that when combined with selenium, CoQ10 slashed the death rate from cardiovascular disease by more than half!44 The science is so strong that one of the study authors proclaimed CoQ10 to be a “scientific breakthrough in the management of chronic heart failure.”45
CoQ10 has two primary ways of protecting mitochondria from age-related decay and death. First, it plays an essential role in the electron transport chain, facilitating the efficient transfer of electrons into ATP.46 Second, it acts as a powerful scavenger of free radicals, neutralizing their lethal action and dramatically reducing oxidative damage.46
As a result, CoQ10 offers a powerful way to help slow, or even reverse, a natural aging process by restoring youthful mitochondrial protection against free radicals.47,48
There’s just one problem. CoQ10 can quickly become depleted in the body because it donates its own electrons in order to neutralize the flood of free radicals. That makes ensuring the body’s continued supply of CoQ10 critical.
And that’s why there continues to be so much excitement about shilajit. While practically unheard of in modern medicine, this ancient Ayurvedic adaptogen has been found to stabilize, revitalize, and preserve CoQ10 in its active (ubiquinol) form, boosting the levels of CoQ10 that are critical for protection against mitochondrial aging.10,14,17,49
When used along with CoQ10, the combination produces benefits above and beyond what each nutrient offers individually, providing a powerful synergistic effect that boosts energy, protects mitochondria, and reduces aging at the cellular level.
As you’re about to read, one particular breakthrough study demonstrates this perfectly.
Powerful Duo Produces Dramatic Results
A team of researchers published a compelling study showing how shilajit plus CoQ10 preserves and protects energy function.10 The researchers engaged mice in strenuous and stressful physical activity for two hours each day for seven days.
Subjecting laboratory animals to obligatory exercise is one of the most direct ways to study energy balance. In a forced swim test, the animals swim to a state of exhaustion, and their blood is drawn both before and after exercise to measure energy markers. In unsupplemented animals, the expected outcome is a reduction in ATP, as mitochondria reach their maximum ability to produce it.
For this study, the animals were divided into groups that either received no supplements, CoQ10 alone, shilajit alone, or a combination of both shilajit and CoQ10.10 After subjecting the mice to the forced swim test, the researchers measured the ATP content in muscle, brain, and blood.
The unsupplemented group showed significant reductions in ATP content of muscle, brain, and blood. This was expected, since the exercise demanded ATP for energy, which was eventually exhausted as mitochondria failed to keep up.
Remarkably, all three supplemented groups maintained higher levels of ATP in muscle, brain, and blood. Individually, both shilajit and CoQ10 by themselves produced significant elevations of ATP compared with the unsupplemented animals. But the key discovery was that the combination of these two nutrients had a synergistic effect, producing greater ATP recovery than seen with either nutrient alone.
In fact, in the brain and blood, the shilajit/CoQ10 combination brought ATP levels back nearly to those of un-exercised control animals! As an added benefit, supplementation with shilajit prevented significant drops in CoQ10 levels in the blood of exercised mice.
Ultimately, the synergistic effects of shilajit plus CoQ10 offer an unparalleled option to protect mitochondrial DNA and combat aging.
In a similar experiment, mice were induced to develop chronic fatigue syndrome by undergoing daily forced swimming for 21 days, and then subjected to a series of stress tests that evaluated their mobility and anxiety levels.50 Shilajit was administered prior to the induction of chronic fatigue syndrome in some of the animals.
The results of this study showed that unsupplemented animals experienced prolonged immobility, decreased climbing behaviors, and increased anxiety. Supplemented mice did not demonstrate these deleterious changes. The supplemented animals also showed no signs of the chronic fatigue syndrome-induced mitochondrial oxidative stress seen in control animals. This study provides further demonstration of shilajit’s energy-boosting capabilities, and hints at the exciting neuro-behavioral effects seen in other studies.
Why Such Dramatic Results?
The answer lies in components found in shilajit that work synergistically with CoQ10 such as fulvic acid and related humic substances.
Fulvic acid stimulates mitochondrial energy transfer and makes mitochondrial extraction of energy more efficient,51 while humic substances speed the transfer of electrons along the electron transport chain, enhancing its efficiency.52-55
Ultimately, these actions give shilajit properties similar to a fuel supplement for a car engine: They make the entire energy-production apparatus run more efficiently, with fewer waste products and destructive effects. This keeps mitochondria in a youthful, more potent condition that allows them to deliver cleaner energy, in larger amounts, and with less wear and tear. This powerfully opposes the age-promoting effects of mitochondrial burnout.
Shilajit’s energy-boosting, mitochondrial-protecting capabilities translate into meaningful results in animal studies of two of the body’s biggest energy-consumers: the brain and heart.
Shilajit and the Aging Brain
One devastating consequence of mitochondrial aging and loss of ATP production is deterioration of the central nervous system function.
In fact, poor mitochondrial energy production is considered both a cause and a consequence of memory loss and neurodegenerative diseases like Alzheimer’s and Parkinson’s.56-58 A growing body of evidence shows that shilajit has the potential to reverse many of these neurological changes.
Numerous studies have shown that shilajit fights Alzheimer’s on multiple fronts. First, the neurotransmitter acetylcholine is known to be deficient in patients with Alzheimer’s disease. Acetylcholine is a brain chemical that is important for memory and attention. It is believed that maintaining healthy acetylcholine could help prevent the worsening of Alzheimer’s symptoms. That’s where shilajit comes in: It helps produce a beneficial increase in acetylcholine in the brain by reducing levels of an enzyme that breaks it down.59
Another hallmark of Alzheimer’s disease is the buildup of abnormal proteins called tau (within brain cells) and beta-amyloid (outside of cells), which appear to induce neuronal dysfunction and early cell death. Inhibiting these abnormal protein deposits is a promising target of Alzheimer’s drug therapy, though no drug has yet emerged that effectively reduces such aggregates.60,61
But shilajit has succeeded where drugs have failed: Lab studies demonstrate that one of the principal substances in shilajit (fulvic acid) inhibits the buildup of dangerous tau proteins. It even goes one step beyond that. In an exciting discovery, shilajit was found to significantly untangle filaments of the offending protein, an apparent reversal of the progression of Alzhiemer’s!60,61
Shilajit exerts beneficial effects on Parkinson’s disease by increasing levels of essential neurotransmitters (brain signaling molecules) such as dopamine, which is reduced in Parkinson’s. In addition, an early study on rats in mazes showed that shilajit significantly improved performance and reduced anxiety levels.62
Shilajit and Heart Function
Ayurvedic practitioners have traditionally used shilajit as a treatment for hypertension and improving heart function.63 Recent studies have validated shilajit’s heart-healthy benefits, specifically for those with high blood pressure or other cardiac stressing conditions.
The first study evaluated a tiny marine organism called Daphnia. Although they are invertebrates, Daphnia have hearts that respond similarly to those of humans when exposed to a variety of cardiac medications, making them an ideal test organism.63 When Daphnia were treated with low doses of shilajit, their heart rates fell significantly, an effect frequently sought in patients with high blood pressure or other cardiac stressing conditions, suggesting a use for shilajit in humans with these conditions.63
Similar reductions in heart rate and blood pressure were seen in laboratory rats. One particular study showed that shilajit has important effects that mimic the parasympathetic nervous system. This is the system that goes into action to induce the opposite of the “fight-or-flight” reflex, producing a state of calm, with low heart rate and blood pressure.64 Healthy rats treated with shilajit showed significant reductions in blood pressure, heart rate, and respiratory rate, suggesting a beneficial energy-conserving status.64
Many people are excited to learn that shilajit helps protect against the kind of heart muscle injury that occurs during a heart attack. This was demonstrated in a study of rats that were divided into two groups: one served as a control group and the other received shilajit supplementation for seven days prior to treatment with a drug (isoproterenol) that induces heart muscle injury.65
Following treatment with isoproterenol, unsupplemented animals developed areas of heart muscle damage and a loss of pressure generated by heart contractions. By contrast, shilajit-supplemented rats maintained pumping pressure, had smaller and less severe areas of muscle damage, and displayed lower levels of injury-marking heart muscle enzymes.65
Mitochondrial dysfunction is linked to a broad range of degenerative illness, from diabetes and neurological disorders to heart and kidney failure.
Shilajit helps combat mitochondrial dysfunction-induced aging. Working synergistically with CoQ10, shilajit boosts energy, protects mitochondria, and reduces aging at the cellular level.
Studies show that shilajit acts like a fuel supplement in a race car, boosting efficiency and reducing wear and tear on essential structures. These effects are showing great promise in preventing the aging of energy-intensive tissues like the heart and brain.
Most readers of this magazine have enjoyed the synergistic effects of shilajit and ubiquinol CoQ10 for the past eight years in the supplements they use daily.
If you have any questions on the scientific content of this article, please call a Life Extension® Wellness Specialist at 1-866-864-3027.
- Duberley KE, Abramov AY, Chalasani A, et al. Human neuronal coenzyme Q10 deficiency results in global loss of mitochondrial respiratory chain activity, increased mitochondrial oxidative stress and reversal of ATP synthase activity: implications for pathogenesis and treatment. J Inherit Metab Dis. 2013 Jan;36(1):63-73.
- Fernández-Ayala DJ, López-Lluch G, García-Valdés M, et al. Specificity of coenzyme Q10 for a balanced function of respiratory chain and endogenous ubiquinone biosynthesis in human cells. Biochim Biophys Acta. 2005;1706:174-83.
- López-Martín JM, Salviati L, Trevisson E, et al. Missense mutation of the COQ2 gene causes defects of bioenergetics and de novo pyrimidine synthesis. Hum Mol Genet. 2007;16:1091-7.
- Cordero MD, Cotán D, del-Pozo-Martín Y, et al. Oral coenzyme Q10 supplementation improves clinical symptoms and recovers pathologic alterations in blood mononuclear cells in a fibromyalgia patient. Nutrition. 2012 Nov-Dec;28(11-12):1200-3.
- Takahashi M, Ogawara M, Shimizu T, Shirasawa T. Restoration of the behavioral rates and lifespan in clk-1 mutant nematodes in response to exogenous coenzyme Q(10). Exp Gerontol. 2012 Mar;47(3):276-9.
- Ishii N, Senoo-Matsuda N, Miyake K, et al. Coenzyme Q10 can prolong C. elegans lifespan by lowering oxidative stress. Mech Ageing Dev. 2004 Jan;125(1):41-6.
- Janson M. Orthomolecular medicine: the therapeutic use of dietary supplements for anti-aging. Clin Interv Aging. 2006;1(3):261-5.
- Ochoa JJ, Quiles JL, Lopez-Frias M, et al. Effect of lifelong coenzyme Q10 supplementation on age-related oxidative stress and mitochondrial function in liver and skeletal muscle of rats fed on a polyunsaturated fatty acid (PUFA)-rich diet. J Gerontol A Biol Sci Med Sci. 2007;62(11):1211-8.
- Valero T. Mitochondrial biogenesis: pharmacological approaches. Curr Pharm Des. 2014;20(35):5507-9.
- Bhattacharyya S, Pal D, Gupta AK, et al. Beneficial effect of processed shilajit on swimming exercise induced impaired energy status of mice. Pharmacologyonline. 2009;1:817-25.
- Available at: http://lifespa.com/ayurvedic-supplement-facts/shilajit/. Accessed October 22, 2015.
- Bhattacharyya S, Pal D, Banerjee D. Shilajit dibenzo—pyrones: mitochondria targeted antioxidants. Pharmacology online. 2009;2:690-8.
- Agarwal SP, Khanna R, Karmarkar R, et al. Shilajit: a review. Phytother Res. 2007 May;21(5):401-5.
- Bhattacharya SK, Bhattacharya A, Chakrabarti A. Adaptogenic activity of Siotone, a polyherbal formulation of Ayurvedic rasayanas . Indian J Exp Biol. 2000 Feb;38(2):119-28.
- Goel RK, Banerjee RS, Acharya SB. Antiulcerogenic and antiinflammatory studies with shilajit. J Ethnopharmacol. 1990 Apr;29(1):95-103.
- Park JS, Kim GY, Han K. The spermatogenic and ovogenic effects of chronically administered Shilajit to rats. J Ethnopharmacol. 2006 Oct 11;107(3):349-53.
- Ghosal S. Shilajit in Perspective. Oxford, U.K.: Narosa Publishing House; 2006.
- Malekzadeh G, Dashti-Rahmatabadi MH, Zanbagh S, et al. Mumijo attenuates chemically induced inflammatory pain in mice. Altern Ther Health Med. 2015 Mar-Apr;21(2):42-7.
- De Pauw A, Tejerina S, Raes M, Keijer J, Arnould T. Mitochondrial (dys)function in 15. adipocyte (de)differentiation and systemic metabolic alterations. Am J Pathol. 2009 Sep;175(3):927-39.
- Conley KE, Amara CE, Jubrias SA, Marcinek DJ. Mitochondrial function, fibre types and ageing: new insights from human muscle in vivo. Exp Physiol. 2007 Mar;92(2):333-9.
- Lesnefsky EJ, Moghaddas S, Tandler B, Kerner J, Hoppel CL. Mitochondrial dysfunction in cardiac disease: ischemia—reperfusion, aging, and heart failure. J Mol Cell Cardiol. 2001 Jun;33(6):1065-89.
- Barja G. Free radicals and aging. Trends Neurosci. 2004 Oct;27(10):595-600.
- Hekimi S, Lapointe J, Wen Y. Taking a “good” look at free radicals in the aging process. Trends Cell Biol. 2011 Oct;21(10):569-76.
- Liochev SI. Reactive oxygen species and the free radical theory of aging. Free Radic Biol Med. 2013 Jul;60:1-4.
- Sinha K, Das J, Pal PB, et al. Oxidative stress: the mitochondria-dependent and mitochondria-independent pathways of apoptosis. Arch Toxicol. 2013 Jul;87(7):1157-80.
- Birben E, Sahiner UM, Sackesen C, Erzurum S, Kalayci O. Oxidative stress and antioxidant defense. World Allergy Organ J. 2012 Jan;5(1):9-19.
- Wei YH, Lu CY, Lee HC, et al. Oxidative damage and mutation to mitochondrial DNA and age-dependent decline of mitochondrial respiratory function. Ann NY Acad Sci. 1998 Nov 20;854:155-70.
- Mandavilli BS, Santos JH, Van Houten B. Mitochondrial DNA repair and aging. Mutat Res. 2002 Nov 30;509(1-2):127-51.
- Cadenas E, Davies KJ. Mitochondrial free radical generation, oxidative stress, and aging. Free Radic Biol Med. 2000 Aug;29(3-4):222-30.
- Wei YH, Lee HC. Oxidative stress, mitochondrial DNA mutation, and impairment of antioxidant enzymes in aging. Exp Biol Med (Maywood). 2002 Oct;227(9):671-82.
- Hamilton ML, Van Remmen H, Drake JA, et al. Does oxidative damage to DNA increase with age? PNAS. 2001;98(18):10469-74.
- Linnane AW, Marzuki S, Ozawa T, Tanaka M. Mitochondrial DNA mutations as an important contributor to ageing and degenerative diseases. Lancet. 1989;1(8639):642-5.
- Rolo AP, Palmeira CM. Diabetes and mitochondrial function: role of hyperglycemia and oxidative stress. Toxicol Appl Pharmacol. 2006 Apr 15;212(2):167-78.
- Picard M, Turnbull DM. Linking the metabolic state and mitochondrial DNA in chronic disease, health, and aging. Diabetes. 2013 Mar;62(3):672-8.
- Scheffler K, Krohn M, Dunkelmann T, et al. Mitochondrial DNA polymorphisms specifically modify cerebral—amyloid proteostasis. Acta Neuropathol. 2012 Aug;124(2):199-208.
- Maruszak A, Zekanowski C. Mitochondrial dysfunction and Alzheimer’s disease. Prog Neuropsychopharmacol Biol Psychiatry. 2011 Mar 30;35(2):320-30.
- Lanza IR, Nair KS. Mitochondrial function as a determinant of life span. Pflugers Arch. 2010 Jan;459(2):277-89.
- Robb EL, Page MM, Stuart JA. Mitochondria, cellular stress resistance, somatic cell depletion and lifespan. Curr Aging Sci. 2009 Mar;2(1):12-27.
- Alexeyev MF, LeDoux SP, Wilson GL. Mitochondrial DNA and aging. Clin Sci (Lond). 2004 Oct;107(4):355-64.
- Quiles JL, Ochoa JJ, Huertas JR, Mataix J. Coenzyme Q supplementation protects from age-related DNA double-strand breaks and increases lifespan in rats fed on a PUFA-rich diet. Exp Gerontol. 2004 Feb;39(2):189-94.
- Available at: http://www.cdc.gov/nchs/fastats/life-expectancy.htm. Accessed September 9, 2015.
- Sander S, Coleman CI, Patel AA, et al. The impact of coenzyme Q10 on systolic function in patients with chronic heart failure. J Card Fail. 2006 Aug;12(6):464-72.
- Dai YL, Luk TH, Yiu KH, et al. Reversal of mitochondrial dysfunction by coenzyme Q10 supplement improves endothelial function in patients with ischaemic left ventricular systolic dysfunction: a randomized controlled trial. Atherosclerosis. 2011 Jun;216(2):395-401.
- Alehagen U, Johansson P, Bjornstedt M, et al. Cardiovascular mortality and N-terminal-proBNP reduced after combined selenium and coenzyme Q10 supplementation: A 5-year prospective randomized double-blind placebo-controlled trial among elderly Swedish citizens. Int J Cardiol. 2013 Sep 1;167(5):1860-6.
- Mortensen SA, et al. Coenzyme Q10: clinical benefits with biochemical correlates suggesting a scientific breakthrough in the management of chronic heart failure. Int J Tissue React. 1990;12(3):155-62.
- Sohal RS, Forster MJ. Coenzyme Q, oxidative stress and aging. Mitochondrion. 2007 Jun;7 Suppl:S103-11.
- Karbowski M, Neutzner A. Neurodegeneration as a consequence of failed mitochondrial maintenance. Acta Neuropathol. 2012 Feb;123(2):157-71.
- Lenaz G, Bovina C, D’Aurelio M, et al. Role of mitochondria in oxidative stress and aging. Ann N Y Acad Sci. 2002 Apr;959:199-213.
- Aminul I, Runa G, Dipankar B, et al. Biotransformation of 3-hydroxydibenzo—pyrone into 3,8 dihydroxydibenzo—pyrone and aminoacyl conjugates by Aspergillus niger isolated from native shilajit. Electron J Biotechnol. 2008;11(3).
- Surapaneni DK, Adapa SR, Preeti K, Teja GR, Veeraragavan M, Krishnamurthy S. Shilajit attenuates behavioral symptoms of chronic fatigue syndrome by modulating the hypothalamic-pituitary-adrenal axis and mitochondrial bioenergetics in rats. J Ethnopharmacol. 2012 Aug 30;143(1):91-9.
- Visser SA. Effect of humic substances on mitochondrial respiration and oxidative phosphorylation. Sci Total Environ. 1987 Apr;62:347-54.
- Klapper L, McKnight DM, Fulton JR, et al. Fulvic acid oxidation state detection using fluorescence spectroscopy. Environ Sci Technol. 2002 Jul 15;36(14):3170-5.
- Royer RA, Burgos WD, Fisher AS, et al. Enhancement of biological reduction of hematite by electron shuttling and Fe(II) complexation. Environ Sci Technol. 2002 May 1;36(9):1939-46.
- Kang SH, Choi W. Oxidative degradation of organic compounds using zero-valent iron in the presence of natural organic matter serving as an electron shuttle. Environ Sci Technol. 2009 Feb 1;43(3):878-83.
- Dantas JM, Kokhan O, Pokkuluri PR, Salgueiro CA. Molecular interaction studies revealed the bifunctional behavior of triheme cytochrome PpcA from Geobacter sulfurreducens toward the redox active analog of humic substances. Biochim Biophys Acta. 2015 Jun 9;1847(10):1129-38.
- Fernandez-Moriano C, Gonzalez-Burgos E, Gomez-Serranillos MP. Mitochondria-Targeted Protective Compounds in Parkinson’s and Alzheimer’s Diseases. Oxid Med Cell Longev. 2015;2015:408927.
- Hroudova J, Singh N, Fisar Z. Mitochondrial dysfunctions in neurodegenerative diseases: relevance to Alzheimer’s disease. Biomed Res Int. 2014;2014:175062.
- Picone P, Nuzzo D, Caruana L, Scafidi V, Di Carlo M. Mitochondrial dysfunction: different routes to Alzheimer’s disease therapy. Oxid Med Cell Longev. 2014;2014:780179.
- Schliebs R, Liebmann A, Bhattacharya SK, et al. Systemic administration of defined extracts from Withania somnifera (Indian Ginseng) and Shilajit differentially affects cholinergic but not glutamatergic and GABAergic markers in rat brain. Neurochem Int. 1997 Feb;30(2):181-90.
- Guzman-Martinez L, Farias GA, Maccioni RB. Tau oligomers as potential targets for Alzheimer’s diagnosis and novel drugs. Front Neurol. 2013;4:167.
- Cornejo A, Jimenez JM, Caballero L, Melo F, Maccioni RB. Fulvic acid inhibits aggregation and promotes disassembly of tau fibrils associated with Alzheimer’s disease. J Alzheimers Dis. 2011;27(1):143-53.
- Jaiswal A K, Bhattacharya S K. Effects of Shilajit on memory, anxiety and brain monoamines in rats. Indian J Pharmacol 1992;24(1):12-7.
- Gaikwad NS, Panat AV, Deshpande MS, Ramya K, Khalid PU, Augustine P. Effect of shilajit on the heart of Daphnia: A preliminary study. J Ayurveda Integr Med. 2012 Jan;3(1):3-5.
- Kaur S, Kumar P, Kumar D, Kharya MD, Singh N. Parasympathomimetic effect of shilajit accounts for relaxation of rat corpus cavernosum. Am J Mens Health. 2013 Mar;7(2):119-27.
- Joukar S, Najafipour H, Dabiri S, Sheibani M, Sharokhi N. Cardioprotective effect of mumie (shilajit) on experimentally induced myocardial injury. Cardiovasc Toxicol. 2014 Sep;14(3):214-21.
- Hagen TM, Ingersoll RT, Lykkesfeldt J, et al. (R)-alpha-lipoic acid-supplemented old rats have improved mitochondrial function, decreased oxidative damage, and increased metabolic rate. FASEB J. 1999 Feb;13(2):411-8.
- DiMauro S, Tanji K, Bonilla E, Pallotti F, Schon EA. Mitochondrial abnormalities in muscle and other aging cells: classification, causes, and effects. Muscle Nerve. 2002 Nov;26(5):597-607.
- Choksi KB, Nuss JE, Boylston WH, Rabek JP, Papaconstantinou J. Age-related increases in oxidatively damaged proteins of mouse kidney mitochondrial electron transport chain complexes. Free Radic Biol Med. 2007 Nov 15;43(10):1423-38.
- Sullivan PG, Brown MR. Mitochondrial aging and dysfunction in Alzheimer’s disease. Prog Neuropsychopharmacol Biol Psychiatry. 2005 Mar;29(3):407-10.
- Rosenfeldt FL, Pepe S, Ou R, et al. Coenzyme Q10 improves the tolerance of the senescent myocardium to aerobic and ischemic stress: studies in rats and in human atrial tissue. Biofactors. 1999;9(2-4):291-9.
- Kalen A, Appelkvist EL, Dallner G. Age-related changes in the lipid compositions of rat and human tissues. Lipids. 1989;24(7):579-84.
- Hoppe U, Bergemann J, Diembeck W, et al. Coenzyme Q10, a cutaneous antioxidant and energizer. Biofactors. 1999;9(2-4):371-8.