By: Dr. Xavier Figueroa
“You know, people get frustrated because their loved ones who have Alzheimer’s, oh, he doesn’t recognize me anymore, how can I recognize this person, if they don’t recognize me? They’re not the same person. “ “Well, they are the same person, but they’ve got a brain disease. And it’s not their fault they’ve got this disease.” –Ron Reagan—
The disease that bears the name of Aloysius Alzheimer was first described in Munich, 1906. Prior to this discovery by Dr. Alzheimer, the loss of memory, forgetfulness, and the decline in mental acuity and competence were ascribed to old age. Since that time, the clinical symptoms and the changes that occur in the brain are known as a neurological disease and not the inevitable decline of the aging process.
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These changes are well documented, with a variety of different types of dementia now understood to be part of a spectrum of disease. In the last 105 years, the biological mechanisms that kill the neurons of the brain have become defined (1-3), but the ultimate cause remains elusive. Recently, the role of the amyloid plaques (4-7) and neurofibrillary tangles (8-13), a hallmark of Alzheimer ’s disease (AD), have been redefined. Previous work assumed that plaques and tangles were the cause of AD, but it appears that these proteins are the brain’s response to the actual damaging agent of the disease: oxygen radical formation (14-18).
Fight Oxygen With…Oxygen!?
Hyperbaric oxygen therapy (HBOT) has been in use for over 100 years, safely treating a variety of medical conditions (19-21). HBOT is a treatment in which the entire body is exposed to 100% oxygen under increased pressure. By augmenting total gas pressure, oxygen levels in all body organs can be increased dramatically (19, 21), sparing and maintaining organs that are oxygen deprived, removing obstructions in blood flow caused by gas bubbles, and inhibiting certain types of bacteria (22-24).
The ability of HBOT to help in the healing process is mediated by a number of different mechanisms in the body. Each of these mechanisms helps us understand why HBOT can accelerate wound healing and help in combating a variety of neurological diseases. In animal and human clinical studies, HBOT has shown a beneficial effect in reducing inflammation (25-28) in stroke and headtrauma. This anti-inflammatory effect helps to reduce swelling and increase healthy blood flow to the brain. At the same time, HBOT promotes the growth of new blood vessels, increases the number of circulating stem cells that are involved in new blood vessel growth and wound healing (29-31), and induces the production of new neurons in the brain (32-34).
As the section title implies, the idea of using oxygen to fight oxygen radicals seems like a bad idea. Why give more of the same material that produces the damaging oxygen radicals? Studies looking into this question reveal that HBOT exposure increases the activity and number of oxygen radical-fighting enzymes (35-39). By giving more oxygen, oxygen radicals are suppressed and a number of healing and rejuvenating pathways are stimulated.
What Can HBOT Do in Alzheimer’s Disease?
Inflammation is a hallmark of AD and plays an important role in the damage caused by this disease. For three decades, non-steroidal anti-inflammatory drugs (NSAIDs: aspirin, acetaminophen, ibuprofen) have been known to reduce the severity of AD (40-45). Research studies of brain trauma have found that inflammation can be further reduced and controlled by use of HBOT (25, 26, 46). The hyperbaric oxygen effect on inflammation could help reduce and reverse the damage seen in AD.
Since the early 1990s, the idea of insufficient blood flow in the brain was a major impetus for developing therapies that could stimulate new blood vessel growth in the brain of AD sufferers. This new blood vessel growth, called angiogenesis, has been shown to be effective as a critical component for fighting the ravages of AD.
A tissue known for its angiogenesis-inducing capabilities is the omentum, a lining of the intestine that is routinely used with compromised surgical sections (47). Reports of omentum transplantation into the brains of AD patients (48-53) demonstrated a reversal of symptoms associated with AD, and reduction in senile plaques was observed (49, 54, 55) where the omentum was transplanted onto the brain. The major limitation with this surgical procedure is its severity and the lack of long-term effectiveness (54). The surgery is highly invasive (the skull and the abdomen are opened) and risky, given the age and poor health condition of many AD sufferers. Yet, many are willing to risk it due to the lack of options and the positive outcomes that do arise from it. Even short-term benefits do provide a reprieve from the ravages of AD.
In HBOT, the induction of blood vessel regrowth is observed in the brain (43) and has successfully helped to treat traumatic brain injury (56-60). It is not unreasonable to think that with HBOT, the effects seen with omental transplantation could be replicated with AD sufferers. The approach of inducing angiogenesis with HBOT obviates the risky surgical approach and the required recovery after surgery. Testing for functional cognitive recovery can be done continuously, without the need to wait for recovery, as well.
At the same time, inflammation can be readily reduced in the brain via HBOT (25-28, 46, 61), providing another healing effect. The work done with NSAIDS clearly shows that inflammation plays an important role in AD. By reducing the level of inflammation, blood vessels and new neurons may grow faster in the brain and promote a quicker recovery.
Finally, since AD is a disease caused by oxygen radicals (15, 17, 42), the increase in anti-oxidant enzyme activity by HBOT treatments could provide a third healing effect (37, 62). The role of oxygen radicals in producing the damage in the brain may be countered by improving mitochondrial function. HBOT has shown the ability to return “idling” mitochondria to full function, hopefully reducing the number of mitochondria that are over producing oxygen radicals.
Why Isn’t HBOT Used On AD?
The use of hyperbaric oxygen for neurological diseases is a relatively new experimental application. For decades, the medical community has been overly concerned about the production of oxygen radicals due to HBOT (63). Recent studies have demonstrated that this concern is minor (64-66), and the increase in oxygen radical-fighting enzymes more than compensates for the extra oxygen in the body. Most of the work in AD has been centered on increasing blood flow to the brain, controlling inflammation, removing the amyloid plaques from the brain, and sparing brain function of the affected individuals. An evolution in the way that researchers think about AD is bringing about a major change in treatment of this disease. The observation that HBOT can have a regenerative effect on the brain, restore blood supply, decrease inflammation, and increase anti-oxygen radical activity is a compelling case for using HBOT for AD patients. This may be an effective therapy to halt the ravages of AD and help reverse the damage. At a minimum, we hope that HBOT may help slow down the progression of the disease.
- Rocchi A, Orsucci D, Tognoni G, Ceravolo R, & Siciliano G (2009) The role of vascular factors in late-onset sporadic Alzheimer’s disease. Genetic and molecular aspects. (Translated from eng) Curr Alzheimer Res 6(3):224-237 (in eng).
- Pereira C, Agostinho P, Moreira PI, Cardoso SM, & Oliveira CR (2005) Alzheimer’s disease-associated neurotoxic mechanisms and neuroprotective strategies. (Translated from eng) Curr Drug Targets CNS Neurol Disord 4(4):383-403 (in eng).
- Chong ZZ, Li F, & Maiese K (2005) Stress in the brain: novel cellular mechanisms of injury linked to Alzheimer’s disease. (Translated from eng) Brain Res Brain Res Rev 49(1):1-21 (in eng).
- De Felice FG & Ferreira ST (2002) Beta-amyloid production, aggregation, and clearance as targets for therapy in Alzheimer’s disease. (Translated from eng) Cell Mol Neurobiol 22(5-6):545-563 (in eng).
- Greenfield JP, Gross RS, Gouras GK, & Xu H (2000) Cellular and molecular basis of beta-amyloid precursor protein metabolism. (Translated from eng) Front Biosci 5:D72-83 (in eng).
- Hartmann T (1999) Intracellular biology of Alzheimer’s disease amyloid beta peptide. (Translated from eng) Eur Arch Psychiatry Clin Neurosci 249(6):291-298 (in eng).
- Joachim CL & Selkoe DJ (1992) The seminal role of beta-amyloid in the pathogenesis of Alzheimer disease. (Translated from eng) Alzheimer Dis Assoc Disord 6(1):7-34 (in eng).
- Hernandez F & Avila J (2007) Tauopathies. (Translated from eng) Cell Mol Life Sci 64(17):2219-2233 (in eng).
- Kar A, Kuo D, He R, Zhou J, & Wu JY (2005) Tau alternative splicing and frontotemporal dementia. (Translated from eng) Alzheimer Dis Assoc Disord 19 Suppl 1:S29-36 (in eng).
- D’Souza I & Schellenberg GD (2005) Regulation of tau isoform expression and dementia. (Translated from eng) Biochim Biophys Acta 1739(2-3):104-115 (in eng).
- Gong CX, Liu F, Grundke-Iqbal I, & Iqbal K (2005) Post-translational modifications of tau protein in Alzheimer’s disease. (Translated from eng) J Neural Transm 112(6):813-838 (in eng).
- Terwel D, Dewachter I, & Van Leuven F (2002) Axonal transport, tau protein, and neurodegeneration in Alzheimer’s disease. (Translated from eng) Neuromolecular Med 2(2):151-165 (in eng).
- van Slegtenhorst M, Lewis J, & Hutton M (2000) The molecular genetics of the tauopathies. (Translated from eng) Exp Gerontol 35(4):461-471 (in eng).
- Nunomura A, et al. (2006) Neuropathology in Alzheimer’s disease: awaking from a hundred-year-old dream. (Translated from eng) Sci Aging Knowledge Environ 2006(8):pe10 (in eng).
- Moreira PI, et al. (2005) A second look into the oxidant mechanisms in Alzheimer’s disease. (Translated from eng) Curr Neurovasc Res 2(2):179-184 (in eng).
- Aliyev A, et al. (2005) Mitochondria DNA deletions in atherosclerotic hypoperfused brain microvessels as a primary target for the development of Alzheimer’s disease. (Translated from eng) J Neurol Sci 229-230:285-292 (in eng).
- Smith MA, Rottkamp CA, Nunomura A, Raina AK, & Perry G (2000) Oxidative stress in Alzheimer’s disease. (Translated from eng) Biochim Biophys Acta 1502(1):139-144 (in eng).
- Smith MA, et al. (1998) Amyloid-beta deposition in Alzheimer transgenic mice is associated with oxidative stress. (Translated from eng) J Neurochem 70(5):2212-2215 (in eng).
- Edwards ML (2010) Hyperbaric oxygen therapy. Part 1: history and principles. (Translated from eng) J Vet Emerg Crit Care (San Antonio) 20(3):284-288 (in eng).
- Biddle C (2008) Oxygen: the two-faced elixir of life. (Translated from eng) AANA J 76(1):61-68 (in eng).
- Sheridan RL & Shank ES (1999) Hyperbaric oxygen treatment: a brief overview of a controversial topic. (Translated from eng) J Trauma 47(2):426-435 (in eng).
- Gill AL & Bell CN (2004) Hyperbaric oxygen: its uses, mechanisms of action and outcomes. (Translated from eng) QJM 97(7):385-395 (in eng).
- Edwards ML (2010) Hyperbaric oxygen therapy. Part 2: application in disease. (Translated from English) J Vet Emerg Crit Car 20(3):289-297 (in English).
- Bitterman H (2009) Bench-to-bedside review: oxygen as a drug. (Translated from eng) Crit Care 13(1):205 (in eng).
- Wilson HD, Toepfer VE, Senapati AK, Wilson JR, & Fuchs PN (2007) Hyperbaric oxygen treatment is comparable to acetylsalicylic acid treatment in an animal model of arthritis. (Translated from eng) J Pain 8(12):924-930 (in eng).
- Wilson HD, Wilson JR, & Fuchs PN (2006) Hyperbaric oxygen treatment decreases inflammation and mechanical hypersensitivity in an animal model of inflammatory pain. (Translated from English) Brain Research 1098:126-128 (in English).
- Helms AK, Whelan HT, & Torbey MT (2005) Hyperbaric oxygen therapy of cerebral ischemia. (Translated from English) Cerebrovasc Dis 20(6):417-426 (in English).
- Alex J, et al. (2005) Pretreatment with hyperbaric oxygen and its effect on neuropsychometric dysfunction and systemic inflammatory response after cardiopulmonary bypass: a prospective randomized double-blind trial. (Translated from eng) J Thorac Cardiovasc Surg 130(6):1623-1630 (in eng).
- Milovanova TN, et al. (2009) Hyperbaric oxygen stimulates vasculogenic stem cell growth and differentiation in vivo. (Translated from eng) J Appl Physiol 106(2):711-728 (in eng).
- Liu ZJ & Velazquez OC (2008) Hyperoxia, endothelial progenitor cell mobilization, and diabetic wound healing. (Translated from eng) Antioxid Redox Signal 10(11):1869-1882 (in eng).
- Velazquez OC (2007) Angiogenesis and vasculogenesis: inducing the growth of new blood vessels and wound healing by stimulation of bone marrow-derived progenitor cell mobilization and homing. (Translated from eng) J Vasc Surg 45 Suppl A:A39-47 (in eng).
- Zhang XY, et al. (2011) The Role of beta-Catenin Signaling Pathway on Proliferation of Rats Neural Stem Cells After Hyperbaric Oxygen Therapy In Vitro. (Translated from eng) Cell Mol Neurobiol 31(1):101-109 (in eng).
- Zhang T, et al. (2010) Hyperbaric oxygen therapy improves neurogenesis and brain blood supply in piriform cortex in rats with vascular dementia. (Translated from eng) Brain Inj 24(11):1350-1357 (in eng).
- Yang YJ, et al. (2008) Hyperbaric oxygen induces endogenous neural stem cells to proliferate and differentiate in hypoxic-ischemic brain damage in neonatal rats. (Translated from eng) Undersea Hyperb Med 35(2):113-129 (in eng).
- Nemoto EM & Betterman K (2007) Basic physiology of hyperbaric oxygen in brain. (Translated from eng) Neurol Res 29(2):116-126 (in eng).
- Li Q, Li J, Zhang L, Wang B, & Xiong L (2007) Preconditioning with hyperbaric oxygen induces tolerance against oxidative injury via increased expression of heme oxygenase-1 in primary cultured spinal cord neurons. (Translated from eng) Life Sci 80(12):1087-1093 (in eng).
- Nie H, et al. (2006) Hyperbaric oxygen preconditioning induces tolerance against spinal cord ischemia by upregulation of antioxidant enzymes in rabbits. (Translated from eng) J Cereb Blood Flow Metab 26(5):666-674 (in eng).
- Zhilyaev SY, et al. (2003) Hyperoxic vasoconstriction in the brain is mediated by inactivation of nitric oxide by superoxide anions. (Translated from eng) Neurosci Behav Physiol 33(8):783-787 (in eng).
- Rothfuss A & Speit G (2002) Investigations on the mechanism of hyperbaric oxygen (HBO)-induced adaptive protection against oxidative stress. (Translated from eng) Mutat Res 508(1-2):157-165 (in eng).
- Hoozemans JJ, Veerhuis R, Rozemuller JM, & Eikelenboom P (2011) Soothing the inflamed brain: effect of non-steroidal anti-inflammatory drugs on Alzheimer’s disease pathology. (Translated from eng) CNS Neurol Disord Drug Targets 10(1):57-67 (in eng).
- Gorelick PB (2010) Role of inflammation in cognitive impairment: results of observational epidemiological studies and clinical trials. (Translated from eng) Ann N Y Acad Sci 1207:155-162 (in eng).
- Sun AY, Wang Q, Simonyi A, & Sun GY (2010) Resveratrol as a therapeutic agent for neurodegenerative diseases. (Translated from eng) Mol Neurobiol 41(2-3):375-383 (in eng).
- Ray B & Lahiri DK (2009) Neuroinflammation in Alzheimer’s disease: different molecular targets and potential therapeutic agents including curcumin. (Translated from eng) Curr Opin Pharmacol 9(4):434-444 (in eng).
- Giunta B, et al. (2008) Inflammaging as a prodrome to Alzheimer’s disease. (Translated from eng) J Neuroinflammation 5:51 (in eng).
- Vainio H & Morgan G (1997) Aspirin for the second hundred years: new uses for an old drug. (Translated from eng) Pharmacol Toxicol 81(4):151-152 (in eng).
- Vlodavsky E, Palzur E, & Soustiel JF (2006) Hyperbaric oxygen therapy reduces neuroinflammation and expression of matrix metalloproteinase-9 in the rat model of traumatic brain injury. (Translated from eng) Neuropathol Appl Neurobiol 32(1):40-50 (in eng).
- Rafael H (2006) Neural transplantation. (Translated from eng) J Neurosurg 104(2):336-337; author reply 337-338 (in eng).
- Goldsmith HS, Wu W, Zhong J, & Edgar M (2003) Omental transposition to the brain as a surgical method for treating Alzheimer’s disease. (Translated from eng) Neurol Res 25(6):625-634 (in eng).
- Goldsmith HS (2002) Treatment of Alzheimer’s disease by transposition of the omentum. (Translated from eng) Ann N Y Acad Sci 977:454-467 (in eng).
- Goldsmith HS (2001) Role of the omentum in the treatment of Alzheimer’s disease. (Translated from eng) Neurol Res 23(6):555-564 (in eng).
- Rafael H, Mego R, Moromizato P, & Espinoza M (2000) Omental transplantation for Alzheimer’s disease. (Translated from eng) Neurol India 48(4):319-321 (in eng).
- Goldsmith HS (1997) Omental transposition to the brain for Alzheimer’s disease. (Translated from eng) Ann N Y Acad Sci 826:323-336 (in eng).
- Goldsmith HS (1996) Omental transposition for Alzheimer ‘s disease. (Translated from eng) Neurol Res 18(2):103-108 (in eng).
- Shankle WR, et al. (2008) Omentum transposition surgery for patients with Alzheimer’s disease: a case series. (Translated from eng) Neurol Res 30(3):313-325 (in eng).
- Relkin NR, Edgar MA, Gouras GK, Gandy SE, & Goldsmith HS (1996) Decreased senile plaque density in Alzheimer neocortex adjacent to an omental transposition. (Translated from eng) Neurol Res 18(4):291-294; discussion 295-296 (in eng).
- Harch PG, et al. (2010) Hyperbaric Oxygen Therapy Treatment of Chronic Mild-Moderate Blast-Induced Traumatic Brain Injury/Post Concussion Syndrome with Post Traumatic Stress Disorder: Pilot Trial. International Hyperbaric Medical Foundation.
- Wright JK, Zant E, Groom K, Schlegel RE, & Gilliland K (2009) Case report: Treatment of mild traumatic brain injury with hyperbaric oxygen. (Translated from eng) Undersea Hyperb Med 36(6):391-399 (in eng).
- Harch PG, Fogarty EF, Staab PK, & Van Meter K (2009) Low pressure hyperbaric oxygen therapy and SPECT brain imaging in the treatment of blast-induced chronic traumatic brain injury (post-concussion syndrome) and post traumatic stress disorder: a case report. (Translated from eng) Cases J 2:6538 (in eng).
- Lin JW, et al. (2008) Effect of hyperbaric oxygen on patients with traumatic brain injury. (Translated from eng) Acta Neurochir Suppl 101:145-149 (in eng).
- Rockswold SB, Rockswold GL, & Defillo A (2007) Hyperbaric oxygen in traumatic brain injury. (Translated from eng) Neurol Res 29(2):162-172 (in eng).
- James PB (2007) Hyperbaric oxygenation in fluid microembolism. (Translated from eng) Neurol Res 29(2):156- 161 (in eng).
- Godman CA, Joshi R, Giardina C, Perdrizet G, & Hightower LE (2010) Hyperbaric oxygen treatment induces antioxidant gene expression. (Translated from eng) Ann N Y Acad Sci 1197:178-183 (in eng).
- Narkowicz CK, Vial JH, & McCartney PW (1993) Hyperbaric oxygen therapy increases free radical levels in the blood of humans. (Translated from eng) Free Radic Res Commun 19(2):71-80 (in eng).
- Jain KK (2008) Textbook of hyperbaric medicine (Hogrefe & Huber Publishers, Cambridge, MA) 5th Ed.
- Rossignol DA & Rossignol LW (2006) Hyperbaric oxygen therapy may improve symptoms in autistic children. (Translated from eng) Med Hypotheses 67(2):216-228 (in eng).
- Jain KK (2003) Hyperbaric oxygen in acute ischemic stroke. (Translated from eng) Stroke 34(9):e153; author reply e153-155 (in eng).
Alzheimer’s Disease (AD) is a neurological condition characterized by memory loss and cognitive decline. Research by Dr. Xavier Figueroa explores the potential of Hyperbaric Oxygen Therapy (HBOT) in treating AD. Traditionally, AD’s hallmarks were thought to be amyloid plaques and neurofibrillary tangles, but the study suggests these are responses to oxygen radical damage in the brain.
HBOT involves exposing the body to 100% oxygen under pressure, which can increase oxygen levels in organs and has been used to treat various medical conditions for over a century. The study explains how HBOT can accelerate wound healing and address neurological diseases by reducing inflammation, promoting new blood vessel growth, and stimulating neuron production. It also highlights the idea of using oxygen to fight oxygen radicals, demonstrating that HBOT can boost enzymes that counteract radicals.
Regarding AD, the study discusses inflammation’s role and how HBOT’s anti-inflammatory effects could help reduce damage. It explores the idea of inducing new blood vessel growth (angiogenesis) in AD patients using HBOT, which could mirror the positive effects seen with surgical procedures involving omentum transplantation. This approach eliminates the surgical risks. The study suggests that HBOT’s ability to reduce inflammation and enhance antioxidant enzymes could counteract oxygen radical damage, potentially slowing down AD’s progression. While concerns about oxygen radicals have been a barrier, recent research suggests these concerns are minor compared to the potential benefits of HBOT for AD. Overall, the study indicates that HBOT could hold promise in addressing the effects of AD and possibly reversing its damage.