Derleme
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Nöral Yaşlanma ile İlişkili Süreçlerin Nöroplastisite Üzerine Etkisi

Yıl 2022, Cilt: 5 Sayı: 2, 303 - 311, 01.05.2022
https://doi.org/10.19127/bshealthscience.1021574

Öz

Yaşlanma, nöronal plastisite mekanizmalarını doğrudan etkileyen ve hücresel süreçlerdeki değişikliklerle açıklanabilen bilişsel işlevlerdeki gerileme ile ilişkili bir süreçtir. Yaşlanma süreci beyin boyutunda küçülmeye, beyin vasküler sisteminde ve bilişsel işlevlerde bozukluklara sebep olmaktadır. Beyinde gerçekleşen küçülme ile birlikte moleküler seviyeden doku seviyesine kadar her düzeyde işlevsel değişiklikler meydana gelmektedir. Nöral plastisite mekanizmaları bilişsel fonksiyonları düzenlemekte; öğrenme ve hafıza gibi fonksiyonların devamlılığı ve işlevselliği üzerinde önemli bir rol oynamaktadır. İlgili süreçlerde yaşın ilerlemesine bağlı olarak önemli ölçüde azalma gözlenmektedir. Bu derleme çalışması ile doğal yaşlanma sürecinin nöral plastisite üzerine olan etkisi hipokampus, medial temporal lob ve prefrontal korteks yapıları üzerinden; davranışsal, morfolojik, hücresel ve moleküler yönleri ile tartışılarak; yaşlanmanın nöral plastisite üzerindeki etkisi ve yaşlanma ile ilişkili nöropatolojiler incelenecektir.

Kaynakça

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  • Barnes CA. 1979. Memory deficits associated with senescence: a neurophysiological and behavioral study in the rat. J Comp Physiol Psychol, 93.
  • Barnes CA. 1994. Normal aging: regionally specific changes in hippocampal synaptic transmission. Trends Neurosci, 17.
  • Barnes CA, McNaughton BL. 1980. Physiological compensation for loss of afferent synapses in rat hippocampal granule cells during senescence. J Physiol Lond, 309.
  • Barnes CA, Rao G, Foster, T. C, McNaughton, B. L. 1992. Region-specific age effects on AMPA sensitivity: electrophysiological evidence for loss of synaptic contacts in hippocampal field CA1. Hippocampus, 2.
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Effects of Neural Aging Related Processes on Neuroplasticity

Yıl 2022, Cilt: 5 Sayı: 2, 303 - 311, 01.05.2022
https://doi.org/10.19127/bshealthscience.1021574

Öz

Aging is a process associated with decline in cognitive functions that directly affects neuronal plasticity mechanisms and can be explained by changes in cellular processes. The aging process causes a reduction in brain size, disorders in the cerebral vascular system and cognitive functions. With the shrinkage in the brain, functional changes occur at all levels, from the molecular level to the tissue level. Neural plasticity mechanisms regulate cognitive functions; It plays an important role in the continuity and functionality of functions such as learning and memory. A significant decrease is observed in the related processes depending on the aging process. In this review, the effect of aging on neural plasticity and neuropathologies associated with aging will be examined focusing on the hippocampus, medial temporal lobe and prefrontal cortex structures by discussing behavioral, morphological, cellular and molecular aspects.

Kaynakça

  • Bajjalieh SM, Scheller RH. 1995. The biochemistry of neurotransmitter secretion. J Biol Chem, 270: 1971–1974.
  • Ball MJ. 1977. Neuronal loss, neurofibrillary tangles and granulovacuolar degeneration in the hippocampus with ageing and dementia. A quantitative study. Acta Neuropathol Berl, 37.
  • Barnes CA. 1979. Memory deficits associated with senescence: a neurophysiological and behavioral study in the rat. J Comp Physiol Psychol, 93.
  • Barnes CA. 1994. Normal aging: regionally specific changes in hippocampal synaptic transmission. Trends Neurosci, 17.
  • Barnes CA, McNaughton BL. 1980. Physiological compensation for loss of afferent synapses in rat hippocampal granule cells during senescence. J Physiol Lond, 309.
  • Barnes CA, Rao G, Foster, T. C, McNaughton, B. L. 1992. Region-specific age effects on AMPA sensitivity: electrophysiological evidence for loss of synaptic contacts in hippocampal field CA1. Hippocampus, 2.
  • Barnes CA, Rao G, Houston FP. 2000. LTP induction threshold change in old rats at the perforant path–granule cell synapse. Neurobiol Aging, 21.
  • Beard JR, Officer A, De Carvalho IA, Sadana R, Pot AM, Michel JP, Chatterji S. 2016. The World report on ageing and health: A policy framework for healthy ageing. Lancet, 387: 2145–2154.
  • Béjot Y, Garnier P. 2021. Cerebral ischemia. Hormesis Health Disease, 185–200.
  • Blalock EM. 2003. Gene microarrays in hippocampal aging: statistical profiling identifies novel processes correlated with cognitive impairment. J Neurosci, 23.
  • Bohme GA, Bon C, Lemaire M, Reibaud M, Piot O, Stutzmann JM, Blanchard JC. 1993. Altered synaptic plasticity and memory formation in nitric oxide synthase inhibitor-treated rats. Proc Natl Acad Sci USA, 90(19), 9191–9194.
  • Böhme GA, Bon C, Stutzmann JM, Doble A, Blanchard JC. 1991. Possible involvement of nitric oxide in long-term potentiation. European J Pharmacol, 199(3): 379–381.
  • Brizzee KR, Ordy JM, Bartus RT. 1980. Localization of cellular changes within multimodal sensory regions in aged monkey brain: possible implications for age-related cognitive loss. Neurobiol Aging, 1.
  • Brody H. 1955. Organization of the cerebral cortex. III. A study of aging in the human cerebral cortex. J Comp Neurol, 102.
  • Cabeza R, Albert M, Belleville S, Craik FIM, Duarte A, Grady CL, Rajah MN. 2018. Maintenance, reserve and compensation: the cognitive neuroscience of healthy ageing. Nature Rev Neurosci, 19: 701–710.
  • Camandola S, Mattson MP. 2017. Brain metabolism in health, aging, and neurodegeneration. The EMBO J, 36(11): 1474–1492. Cattaneo E, Rigamonti D, Goffredo D, Zuccato C, Squitieri F, Sipione S. 2001, Mart 1. Loss of normal huntingtin function: New developments in Huntington’s disease research. Trends in Neurosci, 24: 182–188.
  • Chang YM, Rosene DL, Killiany RJ, Mangiamele LA, Luebke JI. 2005. Increased action potential firing rates of layer 2/3 pyramidal cells in the prefrontal cortex are significantly related to cognitive performance in aged monkeys. Cereb Cortex, 15.
  • Coleman PD, Flood DG. 1987. Neuron numbers and dendritic extent in normal aging and Alzheimer’s disease. Neurobiol Aging, 8.
  • Devi L, Raghavendran V, Prabhu BM, Avadhani NG, Anandatheerthavarada HK. 2008. Mitochondrial import and accumulation of α-synuclein impair complex I in human dopaminergic neuronal cultures and Parkinson disease brain. J Biol Chem, 283(14): 9089–9100.
  • Dieguez D, Barea-Rodriguez EJ. 2004. Aging impairs the late phase of long-term potentiation at the medial perforant path–CA3 synapse in awake rats. Synapse, 52.
  • Fang EF, Lautrup S, Hou Y, Demares, TG, Croteau DL, Mattson MP, Bohr VA. 2017. NAD+ in aging: Molecular mechanisms and translational implications. Trends in Molec Med, 23: 899–916.
  • Foster TC, Norris CM. 1997. Age-associated changes in Ca2+-dependent processes: relation to hippocampal synaptic plasticity. Hippocampus, 7.
  • Friel DD. 2000. Mitochondria as regulators of stimulus-evoked calcium signals in neurons. Cell Calcium, 28: 307–316.
  • Gallagher M, Rapp PR. 1997. The use of animal models to study the effects of aging on cognition. Annu Rev Psychol, 48.
  • Geinisman Y, Bondareff W, Dodge JT. 1977. Partial deafferentation of neurons in the dentate gyrus of the senescent rat. Brain Res, 134.
  • Geinisman Y, de Toledo-Morrell L, Morrell F. 1986. Loss of perforated synapses in the dentate gyrus: morphological substrate of memory deficit in aged rats. Proc Natl Acad Sci USA, 83.
  • Gilman CP, Mattson MP. 2002. Do apoptotic mechanisms regulate synaptic plasticity and growth-cone motility? Neuro Molec Med, 2: 197–214.
  • Grill JD, Riddle DR. 2002. Age-related and laminar-specific dendritic changes in the medial frontal cortex of the rat. Brain Res, 937.
  • Guo Z, Ersoz A, Butterfield DA, Mattson MP. 2000. Beneficial effects of dietary restriction on cerebral cortical synaptic terminals: Preservation of glucose and glutamate transport and mitochondrial function after exposure to amyloid β-peptide, iron, and 3-nitropropionic acid. J NeuroChem, 75(1): 314–320.
  • Gürer R, Aydın Ş, Gökçe D, Ayaz T, Işık N. 2016. İdiyopatik Parkinson hastalığında serüloplazminin nörodejenerasyonda rolü. Turk Noroloji Derg, 22(1): 19–25.
  • Gurney ME, Cutting FB, Zhai P, Doble A, Taylor CP, Andrus PK, Hall ED. 1996. Benefit of vitamin E, riluzole, and gabapentin in a transgenic model of familial amyotrophic lateral sclerosis. Annals Neurol, 39(2): 147–157.
  • Guzowski JF. 2000. Inhibition of activity-dependent arc protein expression in the rat hippocampus impairs the maintenance of long-term potentiation and the consolidation of long-term memory. J Neurosci, 20.
  • Guzowski JF, McNaughton BL, Barnes CA, Worley PF. 1999. Environment-specific expression of the immediate-early gene Arc in hippocampal neuronal ensembles. Nature Neurosci, 2.
  • Head E. 1995. Spatial learning and memory as a function of age in the dog. Behav Neurosci, 109.
  • Hung CW, Chen YC, Hsieh WL, Chiou SH, Kao CL. 2010, Kasım. Ageing and neurodegenerative diseases. Ageing Res Rev, 9.
  • Jiang HC, Hsu JM, Yen CP, Chao CC, Chen RH, Pan CL. 2015. Neural activity and CaMKII protect mitochondria from fragmentation in aging Caenorhabditis elegans neurons. Proc Natl Acad Sci USA, 112(28): 8768–8773.
  • Jo J, Whitcomb DJ, Olsen KM, Kerrigan TL, Lo SC, Bru-Mercier G, Cho K. 2011. Aβ1-42 inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3β. Nat Neurosci, 14(5): 545–547.
  • Keller JN, Pang Z, Geddes JW, Begley JG, Germeyer A, Waeg G, Mattson MP. 1997. Impairment of glucose and glutamate transport and induction of mitochondrial oxidative stress and dysfunction in synaptosomes by amyloid β- peptide: Role of the lipid peroxidation product 4-hydroxynonenal. J NeuroChem, 69(1): 273–284.
  • Keuker JI, Luiten PG, Fuchs E. 2003. Preservation of hippocampal neuron numbers in aged rhesus monkeys. Neurobiol Aging, 24.
  • Kitagawa K, Matsumoto M, Kuwabara K, Takasawa KI, Tanaka S, Sasaki T, Hori M. 2002. Protective effect of apolipoprotein E against ischemic neuronal injury is mediated through antioxidant action. J Neurosci Res, 68(2): 226–232.
  • Knott EP, Assi M, Rao SNR, Ghosh M, Pearse DD. 2017. Phosphodiesterase inhibitors as a therapeutic approach to neuroprotection and repair. Interl J Molec Sci, 18.
  • Kumar A, Foster TC. 2005. Intracellular calcium stores contribute to increased susceptibility to LTD induction during aging. Brain Res, 1031.
  • Landfield PW. 1988. Hippocampal neuroBiol mechanisms of age-related memory dysfunction. Neurobiol Aging, 9.
  • Li J, Yuan J. 2008. Caspases in apoptosis and beyond. Oncogene, 27: 6194–6206.
  • Li S, Hong S, Shepardson NE, Walsh DM, Shankar GM, Selkoe D. 2009. Soluble oligomers of amyloid β protein facilitate hippocampal long-term depression by disrupting neuronal glutamate uptake. Neuron, 62(6): 788–801.
  • Li Z, Jo J, Jia JM, Lo SC, Whitcomb DJ, Jiao S, Sheng, M. 2010. Caspase-3 activation via mitochondria is required for long-term depression and AMPA receptor internalization. Cell, 141(5): 859–871.
  • Lu C, Wang Y, Furukawa K, Fu W, Ouyang X, Mattson MP. 2006. Evidence that caspase-1 is a negative regulator of AMPA receptor-mediated long-term potentiation at hippocampal synapses. J Neuro Chem, 97(4): 1104–1110.
  • Lyford GL. 1995. Arc, a growth factor and activity-regulated gene, encodes a novel cytoskeleton-associated protein that is enriched in neuronal dendrites. Neuron, 14.
  • Mark RJ, Hensley K, Butterfield DA, Mattson MP. 1995. Amyloid β-peptide impairs ion-motive ATPase activities: Evidence for a role in loss of neuronal Ca2+ homeostasis and cell death. J Neuroscience, 15(9): 6239–6249.
  • Markham JA, Juraska JM. 2002. Aging and sex influence the anatomy of the rat anterior cingulate cortex. Neurobiol Aging, 23.
  • Markowska AL. 1989. Individual differences in aging: behavioral and neurobiology correlates. Neurobiol Aging, 10.
  • Mattson MP. 2009. Roles of the lipid peroxidation product 4-hydroxynonenal in obesity, the metabolic syndrome, and associated vascular and neurodegenerative disorders. Experiment Gerontol, 44: 625–633.
  • Mattson MP, Arumugam TV. 2018. Hallmarks of brain aging: Adaptive and pathological modification by metabolic states. Cell Metabol, 27: 1176–1199.
  • Mattson MP, Duan W, Maswood N. 2002, Nisan. How does the brain control lifespan? Ageing Res Rev, 1: 155–165.
  • Mattson MP, Gleichmann M, Cheng A. 2008, Aralık 10. Mitochondria in Neuroplasticity and Neurological Disorders. Neuron, 60: 748–766.
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Toplam 96 adet kaynakça vardır.

Ayrıntılar

Birincil Dil Türkçe
Konular Klinik Tıp Bilimleri, Sağlık Kurumları Yönetimi
Bölüm Derleme
Yazarlar

İrem Gülfem Albayrak 0000-0003-3218-7060

Elif Mutlu 0000-0002-2580-4043

Yayımlanma Tarihi 1 Mayıs 2022
Gönderilme Tarihi 10 Kasım 2021
Kabul Tarihi 25 Ocak 2022
Yayımlandığı Sayı Yıl 2022 Cilt: 5 Sayı: 2

Kaynak Göster

APA Albayrak, İ. G., & Mutlu, E. (2022). Nöral Yaşlanma ile İlişkili Süreçlerin Nöroplastisite Üzerine Etkisi. Black Sea Journal of Health Science, 5(2), 303-311. https://doi.org/10.19127/bshealthscience.1021574
AMA Albayrak İG, Mutlu E. Nöral Yaşlanma ile İlişkili Süreçlerin Nöroplastisite Üzerine Etkisi. BSJ Health Sci. Mayıs 2022;5(2):303-311. doi:10.19127/bshealthscience.1021574
Chicago Albayrak, İrem Gülfem, ve Elif Mutlu. “Nöral Yaşlanma Ile İlişkili Süreçlerin Nöroplastisite Üzerine Etkisi”. Black Sea Journal of Health Science 5, sy. 2 (Mayıs 2022): 303-11. https://doi.org/10.19127/bshealthscience.1021574.
EndNote Albayrak İG, Mutlu E (01 Mayıs 2022) Nöral Yaşlanma ile İlişkili Süreçlerin Nöroplastisite Üzerine Etkisi. Black Sea Journal of Health Science 5 2 303–311.
IEEE İ. G. Albayrak ve E. Mutlu, “Nöral Yaşlanma ile İlişkili Süreçlerin Nöroplastisite Üzerine Etkisi”, BSJ Health Sci., c. 5, sy. 2, ss. 303–311, 2022, doi: 10.19127/bshealthscience.1021574.
ISNAD Albayrak, İrem Gülfem - Mutlu, Elif. “Nöral Yaşlanma Ile İlişkili Süreçlerin Nöroplastisite Üzerine Etkisi”. Black Sea Journal of Health Science 5/2 (Mayıs 2022), 303-311. https://doi.org/10.19127/bshealthscience.1021574.
JAMA Albayrak İG, Mutlu E. Nöral Yaşlanma ile İlişkili Süreçlerin Nöroplastisite Üzerine Etkisi. BSJ Health Sci. 2022;5:303–311.
MLA Albayrak, İrem Gülfem ve Elif Mutlu. “Nöral Yaşlanma Ile İlişkili Süreçlerin Nöroplastisite Üzerine Etkisi”. Black Sea Journal of Health Science, c. 5, sy. 2, 2022, ss. 303-11, doi:10.19127/bshealthscience.1021574.
Vancouver Albayrak İG, Mutlu E. Nöral Yaşlanma ile İlişkili Süreçlerin Nöroplastisite Üzerine Etkisi. BSJ Health Sci. 2022;5(2):303-11.