The Power Of Youth. How To Tune Our Mind And Body For A Long And Healthy Life

Brain plasticity refers to the ability of the nervous system to change its structure and functions throughout life in response to environmental diversity. The study of neuroplasticity is particularly relevant when it comes to brain aging, recovery from injuries and strokes, and treatment of neurodegenerative diseases such as Alzheimer's and Parkinson's diseases.

Due to neuroplasticity, nerve cells can restore their structure and function, as well as form new synaptic connections. Neuroplasticity is based on two basic processes: the formation of new connections between nerve cells (synaptic plasticity) and the formation of new neurons (neurogenesis).

SYNAPTIC PLASTICITY

In childhood and adolescence, synaptic plasticity is a key property of the brain: the ability to form new connections between neurons helps to learn quickly, to perceive the world. A child's brain forms connections between neurons when encountering a wide variety of information and experiences. As you get older, the number of connections between neurons decreases. This process is called synaptic pruning. The older we get, the more selective our brain becomes in forming connections. It spends resources only on tracing neural pathways for the thoughts we come back to day after day.

Therefore, many adults' brains resemble a "cast" of every day worries. The neural impulses travel along pathways similar to an asphalt road. It takes enough effort and motivation to go off the beaten track and start to "tread" a new path in the neural thicket. At the same time, at any age, repetitive actions gradually lead to the formation of new neural connections.

NEUROGENESIS

It was long believed that the number of nerve cells remained unchanged throughout life: the claim that nerve cells do not regenerate was seen as an axiom. But in recent decades, the findings show that neurogenesis – the production of new neurons by neural stem cells (precursors of all body cells) – is observed in various parts of the brain even in old age.

Scientists from the University of Illinois, after studying postmortem brain tissue of people aged 79 to 99 years, obtained evidence that the formation of new neurons in the hippocampus occurs not only in healthy people but even in patients with cognitive impairment and Alzheimer's disease, although neurogenesis in the latter is significantly reduced compared with older people who do not have cognitive impairment[54].

Neurobiologists from the University of Jyväskylä (Finland) found during experiments in animals that prolonged aerobic exercise increases neurogenesis in the adult brain[55]. The hippocampus of mice that ran long distances showed increased formation of new neurons after eight weeks.

HOW NOT TO LOSE NEUROPLASTICITY IN ADULTHOOD?

Scientists identify three main factors that affect neuroplasticity at any age[56]:

● physical activity;

● intellectual load;

● nutrition.

A meta-analysis conducted by scientists from the University of Toronto (Canada) shows that physical activity increases the concentration of neurotrophic factors, substances that induce neurons to form new connections[57]. Changes can be noticeable after the first session, and the effect lasts for a day or more.

Regular and intensive training maximizes neuroplasticity. However, we can activate the formation of new connections in the brain even with 30-minute walks in which the heart rate reaches 60 % of the maximum, provided, however, that we do it at least three times a week.

A study conducted at Pennsylvania State University (USA) showed that learning a second language leads to anatomical changes in the brain[58]. They are expressed in an increase in the density of gray matter, which indicates the formation of new neurons, as well as in the appearance of more structured white matter bands (connections between nerve cells). These changes, which were observed in both young and old people, indicate the activation of two mechanisms underlying neuroplasticity: neurogenesis and the formation of new synapses.

Researchers from the University of British Columbia (Canada) conducted a meta-analysis of 21 studies, all of which examined the effects of meditation on neuroplasticity[59]. Experts found 123 differences in the brains of people committed to meditative practices. For example, there was a cortex thickening (increased volume of gray matter) in the prefrontal area. This indicates the activation of neurogenesis in the part of the brain responsible for memory, planning, and self-control through meditation.

Among the nutrients that help maintain neuroplasticity in adulthood, scientists highlight the following:

1. FLAVONOIDS – compounds found in tea, berries, onions, and red wine. A diet rich in flavonoids is associated with better preservation of cognitive function in the elderly[60]. Curcumin, which is found in turmeric root and has antidepressant, anti-inflammatory, neuroprotective, and antioxidant effects.

2. RESVERATROL – a substance found in the wine and juice of black grapes. Evidence suggests that consumption of this flavonoid can slow the age-related decline in intellectual abilities[61].

3. OMEGA-3 – a polyunsaturated fatty acid found in large quantities of sea and river fish. Just 300 grams of grilled salmon or 3 grams of fish oil contain the daily norm. Studies suggest that omega-3 fights inflammation and stimulates neuronal growth factors[62].

Based on these studies and others, the team of nutritionist Martha Clare Morris of Rush University Medical Center created the MIND diet to fight Alzheimer's disease. It can reduce the risk of disease by 54 %, which, researchers say, is superior to the Mediterranean diet[63].

The basis of this diet:

1) greens, vegetables and berries, olive oil;

2) beans;

3) whole grains;

4) fish;

5) wine/black grape juice.

The MIND diet also recommends limiting red meat, butter and margarine, cheese, sweets and candy, fried food, and fast food.

NEUROTRANSMITTERS ARE THE LANGUAGE THE BRAIN SPEAKS

Neurotransmitters are chemical substances that transmit signals between two nerve cells or between neurons and other cells in the body. They affect many psychological and physiological functions of the body, as well as mood, memory, learning ability, and concentration, regulate sleep, appetite, and vital signs: heart rate, breathing, digestion features, etc.

Neurotransmitters are often confused with hormones. This is not surprising, because their regulatory functions are very similar, and, in addition, many neurotransmitters have hormone-double: there is dopamine-hormone and dopamine-neurotransmitter, and noradrenaline-neurotransmitter and noradrenaline hormone, etc. Even though these substances have the same chemical formulas, they differently affect the body.

The main difference is that hormones are produced only in the endocrine glands, while neurotransmitters are produced exclusively by neurons. Therefore, the effect of neurotransmitters is limited to the nervous system, and hormones act on the periphery and cannot penetrate the brain they are hindered by the blood-brain barrier.

The difference between hormones and neurotransmitters with the same chemical formula can be seen in noradrenaline. The hormone noradrenaline is produced in the adrenal glands during stress. Its effect is similar to adrenaline, but it has a more pronounced vasoconstrictive effect and has less effect on the heart rate, a less significant effect on the smooth muscles of the intestines, etc. That is, the sphere of influence of the hormone noradrenaline is internal organs. It is controlling the body's response to stress.

At the same time, the neurotransmitter noradrenaline "reigns" in the brain: in stressful situations, it is responsible for the sense of excitement and risk enjoyment, increasing aggression and reducing anxiety. In its more "peaceful" hypostasis, it helps to memorize information better in training.

THE PRINCIPLE OF OPERATION OF NEUROTRANSMITTERS

At what point does the nerve impulse "lose" its electrical nature and "switch" to a chemical one? This occurs when the signal coming from the nerve cell body along the axon reaches an area called the synapse. The synapse is a contact point between the end of one projection and the beginning of another one or the cell membrane to which a signal is to be delivered. Between them, there is a space 10–50 nanometers wide, which is called the synaptic cleft.

The terminal along which the signal came is called presynaptic. Neurotransmitters are synthesized there: they are contained in small vesicles. Their release into the synaptic cleft occurs in response to reaching a threshold action potential, i.e., the nerve impulse shall be characterized by a certain intensity.

Once released, the neurotransmitter enters the synaptic cleft and contacts the receptors on the surface of the "receiving side" projection, the postsynaptic membrane. Receptor activation gives rise to a new nerve impulse, which continues its way (if there is contact between neurons) or causes the desired effect in the cell to which the signal was sent. However, a chemical signal can also inhibit the nerve impulse at the postsynaptic terminal. It depends on what the neurotransmitters do – excite or inhibit.

After the signal transmission from one terminal to the other, the neurotransmitter molecules left in the cleft are either quickly destroyed or "pulled" into the presynaptic terminal through special protein pumps. This is called the principle of neurotransmitter reuptake, and it is used in the creation of some drugs. The effect of many antidepressants is based on blocking the reuptake of the neurotransmitter serotonin, which is responsible for good mood. As a result, serotonin stays in the synaptic cleft longer, having the desired effect.

WHAT ARE NEUROTRANSMITTERS, AND HOW DO THEY AFFECT PEOPLE?

According to the effect that neurotransmitters have on the "receiving" nerve terminal, they are divided into excitatory: they increase the action potential and generate a new impulse, and inhibitory: block the action potential achievement in the postsynaptic nerve ending. Some neurotransmitters, such as dopamine and acetylcholine, can have both stimulatory and suppressive effects, depending on the type of receptors on the postsynaptic membrane.

Next, we will talk about several neurotransmitters that have a powerful effect on various aspects of human life, both physiological and psychological.

DOPAMIN is called the neurotransmitter of winners, and scientists describe it as one of the key factors of internal reinforcement. Its formation helps to remember positive experiences: for example, when a person tastes good food, receives praise, has sex, and achieves a goal. The dopamine release is followed by euphoria: the brain remembers it and motivates the person to have the positive experience again. Dopamine plays an important role in learning processes, and it is also involved in the regulation of muscle function. When dopamine production is impaired, so-called dopamine diseases, like Parkinson's disease and schizophrenia, develop.

Конец ознакомительного фрагмента.

Текст предоставлен ООО «ЛитРес».

Прочитайте эту книгу целиком, купив полную легальную версию на ЛитРес.

Безопасно оплатить книгу можно банковской картой Visa, MasterCard, Maestro, со счета мобильного телефона, с платежного терминала, в салоне МТС или Связной, через PayPal, WebMoney, Яндекс.Деньги, QIWI Кошелек, бонусными картами или другим удобным Вам способом.

Сноски

1

Geroprotectors is the name given to a group of certain substances or therapeutic methods that help to increase longevity. Read more: Fomenko A. N., Proshkina E. N., Fedintsev A. Yu., Tsvetkov V. O., Shaposhnikov M. V., Moskalev A. A. "Potential geroprotectors." – Ed. note.

2

VSH25 is a project to prolong life and preserve health. Read more at vsh25.net. – Ed. note.

3

Accommodation of the eye is its ability to focus on objects at different distances by changing the refractive properties of the lens. – Ed. note.

4

López-Otín C., Blasco M. A., Partridge L., Serrano M., Kroemer G. The hallmarks of aging. Cell. 2013 Jun 6;153(6):1194-217. doi:10.1016/j.cell.2013.05.039. PMID: 23746838; PMCID: PMC3836174.

5

Jin K. Modern Biological Theories of Aging. Aging Dis. 2010 Oct 1;1(2):72–74. PMID: 21132086; PMCID: PMC2995895.

6

Van Heemst D. Insulin, IGF-1 and longevity. Aging Dis. 2010 Oct;1(2):147-57. Epub 2010 Aug 26. PMID: 22396862; PMCID: PMC3295030.

7

Immunosenescence begins at 5–7 years and completes by puberty, but small fragments of active glandular tissue persist throughout a human's life. – Ed. note.

8

Thomas R., Wang W., Su D. M. Contributions of Age-Related Thymic Involution to Immunosenescence and Inflammaging. Immun Ageing. 2020 Jan 20;17:2. doi:10.1186/s12979-020-0173-8. PMID: 31988649; PMCID: PMC6971920.

9

Freitas A. A., de Magalhães J. P. A review and appraisal of the DNA damage theory of aging. Mutat Res. 2011 Jul-Oct;728(1–2):12–22. doi:10.1016/j.mrrev.2011.05.001. Epub 2011 May 10. PMID: 21600302.

10

Yurov Y. B., Iourov I. Y., Monakhov V. V., Soloviev I. V., Vostrikov V. M., Vorsanova S. G. The variation of aneuploidy frequency in the developing and adult human brain revealed by an interphase FISH study. J Histochem Cytochem. 2005 Mar;53(3):385-90. doi:10.1369/jhc.4A6430.2005. PMID: 15750026.

11

Afanas'ev I. Signaling and Damaging Functions of Free Radicals in AgingFree Radical Theory, Hormesis, and TOR. Aging Dis. 2010 Oct;1(2):75–88. Epub 2010 Jul 12. PMID: 22396858; PMCID: PMC3295029.

12

Warner H. R., Hodes R. J., Pocinki K. What does cell death have to do with aging? J Am Geriatr Soc. 1997 Sep;45(9):1140-6. doi:10.1111/j.15325415.1997.tb05981.x. PMID: 9288026.

13

Ontogeny is the individual development of an organism. – Ed. note.

14

Razgonova M. P., Zakharenko A. M., Golokhvast K. S., et al. Telomerase and telomeres in aging theory and chronographic aging theory (Review). Mol Med Rep. 2020;22(3):1679–1694. doi:10.3892/ mmr.2020.11274.

15

Shay J. W., Wright W. E. Telomerase activity in human cancer. Curr Opin Oncol. 1996 Jan;8(1):66–71. doi:10.1097/00001622-199601000-00012. PMID: 8868103.

16

Furman D., Campisi J., Verdin E., et al. Chronic inflammation in the etiology of disease across the life span. Nat Med. 2019;25:1822–1832. doi:10.1038/s41591-019-0675-0.

17

Gomes M. J., Martinez P. F., Pagan L. U., et al. Skeletal muscle aging: influence of oxidative stress and physical exercise. Oncotarget. 2017 Mar 21;8(12):20428-20440.doi:10.18632/oncotarget.14670. PMID: 28099900; PMCID: PMC5386774.

18

Vargas-Mendoza N., Morales-González Á., Madrigal-Santillán E. O., et al. Antioxidant and Adaptative Response Mediated by Nrf2 during Physical Exercise. Antioxidants (Basel). 2019 Jun 25;8(6):196. doi:10.3390/antiox8060196. PMID: 31242588; PMCID: PMC6617290.

19

Brandao C. F. C., de Carvalho F. G., Souza A. O., et al. Physical training, UCP1 expression, mitochondrial density, and coupling in adipose tissue from women with obesity. Scand J Med Sci Sports. 2019 Nov;29(11):1699–1706. doi:10.1111/sms.13514. Epub 2019 Jul 22. PMID: 31282585.

20

Kanaley J. A. Growth hormone, arginine, and exercise. Curr Opin Clin Nutr Metab Care. 2008 Jan;11(1):50-4. doi:10.1097/MCO.0b013e-3282f2b0ad. PMID: 18090659.

21

Lou M., Zong X. F., Wang L. L. Curative treatment of hypertension by physical exercise. Eur Rev Med Pharmacol Sci. 2017 Jul;21(14):3320–3326. PMID: 28770948.

22

Hirshkowitz M., Whiton K., Albert S. M., et al. National Sleep Foundation's sleep time duration recommendations: methodology and results summary. Sleep Health. 2015 Mar;1(1):40–43. doi:10.1016/j. sleh.2014.12.010. Epub 2015 Jan 8. PMID: 29073412.

23

Kwak S., Kim H., Chey J., Youm Y. Feeling How Old I Am: Subjective Age Is Associated With Estimated Brain Age. Front Aging Neurosci. 2018;10:168. Published 2018 Jun 7. doi:10.3389/ fnagi.2018.00168.

24

Stephan Y., Sutin A. R., Terracciano A. Subjective Age and Mortality in Three Longitudinal Samples. Psychosom Med. 2018 Sep;80(7):659–664. doi:10.1097/PSY.0000000000000613. PMID: 29864106; PMCID: PMC6345273.

25

Povedano J. M., Martinez P., Serrano R., et al. Therapeutic effects of telomerase in mice with pulmonary fibrosis induced by damage to the lungs and short telomeres. Elife. 2018;7:e31299. Published 2018 Jan 30. doi:10.7554/eLife.31299.

26

Reich D., Green R., Kircher M., et al. Genetic history of an archaic hominin group from Denisova Cave in Siberia. Nature. 2010;468, 1053–1060. doi:0.1038/nature09710.

27

Venter J. C., Remington K., Heidelberg J. F., et al. Environmental genome shotgun sequencing of the Sargasso Sea. Science. 2004 Apr 2;304(5667):66–74. doi:10.1126/science.1093857.

28

Fraga M. F., Ballestar E., Paz M. F., et al. Epigenetic differences arise during the lifetime of monozygotic twins. Proceedings of the National Academy of Sciences of the United States of America. 2005;102(30), 10604-10609. doi:10.1073/pnas.0500398102.

29

Waterland R. A., Jirtle R. L. Transposable elements: targets for early nutritional effects on epigenetic gene regulation. Mol Cell Biol. 2003;23(15):52935300. doi:10.1128/mcb.23.15.5293–5300.2003.

30

Ornish D., Magbanua M. J., Weidner G., et al. Changes in prostate gene expression in men undergoing an intensive nutrition and lifestyle intervention. Proceedings of the National Academy of Sciences of the United States of America. 2008;105(24), 8369–8374. doi:10.1073/ pnas.0803080105.

31

Rönn T., Volkov P., Davegårdh C., et al. A six months exercise intervention influences the genome-wide DNA methylation pattern in human adipose tissue. PLoS Genet. 2013 Jun;9(6):e1003572. doi:10.1371/journal.pgen.1003572. Epub 2013 Jun 27. PMID: 23825961; PMCID: PMC3694844.

32

Graff M., Scott R. A., Justice A. E., et al. Genome-wide physical activity interactions in adiposity – a meta-analysis of 200,452 adults. PLoS Genet. 2017;13(4):e1006528. doi:10.1371/journal.pgen. 1006528.

33

Massachusetts General Hospital. (2019, November 5). Physical activity may protect against new episodes of depression. Science Daily. www.sciencedaily.com/releases/2019/11/191105113510.htm.

34

Joehanes R., Just A. C., Marioni R. E., et al. Epigenetic Signatures of Cigarette Smoking. Circ Cardiovasc Genet. 2016;9(5):436–447. doi:10.1161/CIRCGENETICS.116.001506.

35

Garaycoechea J., Crossan G., Langevin F., et al. Alcohol and endogenous aldehydes damage chromosomes and mutate stem cells. Nature. 2018;553, 171–177. doi:10.1038/nature25154.

36

Schrott R., Acharya K., Itchon-Ramos N., et al. Cannabis use is associated with potentially heritable widespread changes in autism candidate gene DLGAP2 DNA methylation in sperm. Epigenetics. 2020;15(1–2):161–173. doi:10.1080/15592294.2019.1656158.

37

Slotkin T. A., Skavicus S., Levin E. D., Seidler F. J. Paternal. 9-Tetrahydrocannabinol Exposure Prior to Mating Elicits Deficits in Cholinergic Synaptic Function in the Offspring. Toxicological Sciences. 2020 Apr;174(2), 210–217. doi:10.1093/toxsci/kfaa004.

38

Madaniyazi L., Li S., Li S., Guo Y. Candidate gene expression in response to low-level air pollution. Environ Int. 2020 Jul;140: 105610. doi:10.1016/j.envint.2020.105610. Epub 2020 Apr 2. PMID:32248990.

39

Noniashvili E. M., Grudinina N. A., Kustova V. E., etc. DNA methylation in early mouse embryogenesis influenced by bisphenol A. Ecological genetics. 2017. 15 (3). P. 42–53.

40

Anway M. D., Cupp A. S., Uzumcu M., Skinner M. K. Epigenetic transgenerational actions of endocrine disruptors and male fertility. Science. 2005 Jun 3;308(5727):1466-9. doi:10.1126/science.1108190. Erratum in: Science. 2010 May 7;328(5979):690. PMID: 15933200.

41

Kiecolt-Glaser J. K., Loving T. J., Stowell J. R., et al. Hostile marital interactions, proinflammatory cytokine production, and wound healing. Arch Gen Psychiatry. 2005;62(12):1377–1384. doi:10.1001/ archpsyc.62.12.1377.

42

Sender R., Fuchs S., Milo R. Revised Estimates for the Number of Human and Bacteria Cells in the Body. Published: August 19, 2016. doi:10.1371/journal.pbio.1002533.

43

Spalding K. L., Bhardwaj R. D., Buchholz B. A., Druid H., Frisén J. Retrospective Birth Dating of Cells in Humans. doi:10.1016/j. cell.2005.04.028PlumX Metrics.

44

Kong S., Zhang Y. H., Zhang W. Regulation of Intestinal Epithelial Cells Properties and Functions by Amino Acids. doi:10.1155/2018/ 2819154.

45

Azevedo F. A. C., Carvalho L. R. B., Grinberg L. T., et al. Equal numbers of neuronal and nonneuronal cells make the human brain an isometrically scaled-up primate brain. Published: 18 February 2009 doi:10.1002/cne.21974.

46

Chemical element is a type of atom that has certain chemical properties. The adult body consists of more than 60 chemical elements – Ed. note.

47

Alberts B., Johnson A., Lewis J., et al. Molecular Biology of the Cell. 4th edition. The Chemical Components of a Cell. https://www.ncbi.nlm.nih.gov/books/NBK26883/#A166.

48

Zaidi Z. F. Gender Differences in Human Brain: A Review. The Open Anatomy Journal. 2010;2:37–55. https://benthamopen.com/AB-STRACT/TOANATJ2-37.

49

Von Bartheld C. S., Bahney J., Herculano-Houzel S. The search for true numbers of neurons and glial cells in the human brain: A review of 150 years of cell counting. J Comp Neurol. 2016;524(18):3865–3895. doi:10.1002/cne.24040.

50

Synapses are divided into chemical, electrical, and mixed. – Ed. note.

51

Von Bartheld C. S., Bahney J., Herculano-Houzel S. The search for true numbers of neurons and glial cells in the human brain: A review of 150 years of cell counting. J Comp Neurol. 2016 Dec 15;524(18):3865–3895. doi:10.1002/cne.24040. Epub 2016 Jun 16. PMID: 27187682; PMCID: PMC5063692.

52

The gut-brain axis includes the entire pool of intestinal microorganisms (microbiota), the "intestinal brain" and the central nervous system. – Ed. note.

53

Banks W. A., Reed M. J., Logsdon A. F., et al. Healthy aging and the blood-brain barrier. Nat Aging. 2021;1:243–254. doi:10.1038/s43587-02100043-5.

54

Tobin M. K., Musaraca K., Disouky A., Shetti A., Bheri A., Honer W. G., Kim N., Dawe R. J., Bennett D. A., Arfanakis K., Lazarov O. Human Hippocampal Neurogenesis Persists in Aged Adults and Alzheimer's Disease Patients. Cell Stem Cell. 2019 Jun 6;24(6):974–982.e3. doi:10.1016/j.stem.2019.05.003. Epub 2019 May 23. PMID: 31130513; PMCID: PMC6608595.

55

Nokia M. S., Lensu S., Ahtiainen J. P., Johansson P. P., Koch L. G., Britton S. L., Kainulainen H. Physical exercise increases adult hippocampal neurogenesis in male rats provided it is aerobic and sustained. J Physiol. 2016;594: 1855–1873. doi:10.1113/JP271552.