Neuroscience of aging

The neuroscience of aging is the study of the changes in the nervous system that occur with ageing. Aging is associated with many changes in the central nervous system, such as mild atrophy of the cortex that is considered non-pathological. Aging is also associated with many neurological and neurodegenerative disease such as amyotrophic lateral sclerosis, dementia, mild cognitive impairment, parkinson's disease, and Creutzfeldt–Jakob disease.[1]

Normal Structural and Neural Changes

Neurogenesis occurs very little in adults, only occurring in the hypothalamus and striatum to a small extent in a process called adult neurogenesis. The volume of the brain actually decrease roughly 5% per decade after forty. It is currently unclear why brain volume decreases with age, however, a few causes may include: cell death, decreased cell volume, and changes in synaptic structure. The changes in brain volume is heterogenous across regions with prefrontal cortex receiving the most significant reduction in volume followed in order by the striatum, the temporal lobe, cerebellar vermis, cerebellar hemispheres, and the hippocampus.[2] However, one review found that the amygdala and ventromedial prefrontal cortex remained relatively free of atrophy, which is consistent with the finding of emotional stability occurring with non-pathological aging.[3] Enlargement of the ventricles, sulci and fissures are also common in non-pathological aging.[4]

Changes may also be associated with neuroplasticity, synaptic functionality and voltage gated calcium channels.[5] Increased magnitude of hyperpolarization, possibly a result of dysfunctional calcium regulation, leads to decreased firing rate of neurons and decreased plasticity. This effect is particularly pronounced in the hippocampus of aged animals, and may be an important contributor to age-associated memory deficits. The hyperpolarization of a neuron can be divided into three stages: the fast, medium and slow hyperpolarization. In aged neurons, the medium and slow hyperpolarization phases involve the prolonged opening of calcium-dependent potassium channels. The prolonging of this phase has been hypothesized to be a result of deregulated calcium and hypoactivity of cholinergic, dopaminergic, serotonergic and glutaminergic pathways.[6]

Normal Functional Changes

Episodic memory starts to decline gradually from middle age, while semantic memory increases all the way into early old age and declines thereafter.[7] Older adults tend to engage their prefrontal cortex more often during working memory tasks, possibly to compensate with executive functions. Further impairments of cognitive function associated with aging include decrease in processing speed and inability to focus. A model proposed to account for altered activation posits that decreased neural efficiency driven by amyloid plaques and decreased dopamine functionality lead to compensatory activation.[8] Decreased processing of negative stimuli as opposed to positive stimuli appear in aging, become significant enough to detect even with autonomic nervous responses to emotionally charged stimuli.[9] Aging is also associated with decreased plantar reflex and achilles reflex response. Nerve conductance also decreases during normal aging.[10]

Pathological Changes

Roughly 20% of persons greater than 60 years of age have a neurological disorder, with episodic disorders being the most common followed by extrapyramidal movement disorders, and nerve disorders.[11] Diseases commonly associated with old age include

The misfolding of proteins is a common component of the proposed pathophysiology of many diseases associated with aging, however there is insufficient evidence to prove this. For example, the tau hypothesis to Alzheimer's proposes that tau protein accumulation results in the breakdown neuron cytoskeletons leading to Alzheimer's.[21] Another proposed mechanism for Alzheimer's is related to the accumulation of amyloid beta,.[22] in a similar mechanism to the prion propagation of Creutzfeldt-Jakob disease. Similarly the protein alpha-synuclein is hypothesized to accumulate in Parkinson's and related diseases.[23]

Management

Treatment of an age related neurological disease varies from disease to disease. Modifiable risk factors for dementia include diabetes, hypertension, smoking, hyperhomocysteinemia, hypercholesterolemia, and obesity(which is usually associated with many other risk factors for dementia). Paradoxically, smoking confers protection against Parkinson's disease.[24] Also conferring protective benefits to age related neurological disease in consumption of coffee or caffeine.[25][26][27] Consumption of fruits, fish and vegetables confer protection against dementia, as does a mediterranean diet.[28] Physical exercise significantly lowers the risk of cognitive decline in old age,[29] and is an effective treatment for those with dementia[30][31] and Parkinson's disease.[32][33][34][35]

References

  1. ↑ Brown, Rebecca C.; Lockwood, Alan H.; Sonawane, Babasaheb R. (8 January 2017). "Neurodegenerative Diseases: An Overview of Environmental Risk Factors". Environmental Health Perspectives. 113 (9): 1250–1256. doi:10.1289/ehp.7567. ISSN 0091-6765. PMC 1280411. PMID 16140637.
  2. ↑ Peters, R (8 January 2017). "Ageing and the brain". Postgraduate Medical Journal. 82 (964): 84–88. doi:10.1136/pgmj.2005.036665. ISSN 0032-5473. PMC 2596698. PMID 16461469.
  3. ↑ Mather, Mara (5 October 2015). "The Affective Neuroscience of Aging". Annual Review of Psychology. 67 (1): 213–238. doi:10.1146/annurev-psych-122414-033540. ISSN 1545-2085.
  4. ↑ LeMay, Marjorie (1984). "Radiologic Changes of the Aging Brain and Skull" (PDF). American Journal of Neuroradiology. 5: 269–275.
  5. ↑ Kelly, K. M.; Nadon, N. L.; Morrison, J. H.; Thibault, O.; Barnes, C. A.; Blalock, E. M. (1 January 2006). "The neurobiology of aging". Epilepsy Research. 68 Suppl 1: S5–20. doi:10.1016/j.eplepsyres.2005.07.015. ISSN 0920-1211. PMID 16386406.
  6. ↑ Kumar, Ashok; Foster, Thomas C. (1 January 2007). "Neurophysiology of Old Neurons and Synapses". Brain Aging: Models, Methods, and Mechanisms. CRC Press/Taylor & Francis.
  7. ↑ Peters, R (8 January 2017). "Ageing and the brain". Postgraduate Medical Journal. 82 (964): 84–88. doi:10.1136/pgmj.2005.036665. ISSN 0032-5473. PMC 2596698. PMID 16461469.
  8. ↑ Reuter-Lorenz, Patricia A.; Park, Denise C. (8 January 2017). "Human Neuroscience and the Aging Mind: A New Look at Old Problems". The Journals of Gerontology Series B: Psychological Sciences and Social Sciences. 65B (4): 405–415. doi:10.1093/geronb/gbq035. ISSN 1079-5014. PMC 2883872. PMID 20478901.
  9. ↑ Kaszniak, Alfred W.; Menchola, Marisa (1 January 2012). "Behavioral neuroscience of emotion in aging". Current Topics in Behavioral Neurosciences. 10: 51–66. doi:10.1007/7854_2011_163. ISSN 1866-3370. PMID 21910076.
  10. ↑ Stanton, Biba R. (1 February 2011). "The neurology of old age". Clinical Medicine. 11 (1): 54–56. doi:10.7861/clinmedicine.11-1-54. ISSN 1470-2118.
  11. ↑ Callixte, Kuate-Tegueu; Clet, Tchaleu Benjamin; Jacques, Doumbe; Faustin, Yepnjio; François, Dartigues Jean; Maturin, Tabue-Teguo (17 April 2015). "The pattern of neurological diseases in elderly people in outpatient consultations in Sub-Saharan Africa". BMC Research Notes. 8. doi:10.1186/s13104-015-1116-x. ISSN 1756-0500. PMC 4405818. PMID 25880073.
  12. ↑ Bensimon G, Ludolph A, Agid Y, Vidailhet M, Payan C, Leigh PN (2008). "Riluzole treatment, survival and diagnostic criteria in Parkinson plus disorders: The NNIPPS Study". Brain. 132 (Pt 1): 156–71. doi:10.1093/brain/awn291. PMC 2638696. PMID 19029129.
  13. ↑ Carroll, William M. (2016). International Neurology. John Wiley & Sons. p. 188. ISBN 9781118777367.
  14. ↑ Mendez MF (November 2012). "Early-onset Alzheimer's disease: nonamnestic subtypes and type 2 AD". Archives of Medical Research. 43 (8): 677–85. doi:10.1016/j.arcmed.2012.11.009. PMC 3532551. PMID 23178565.
  15. ↑ Vermeer SE, Koudstaal PJ, Oudkerk M, Hofman A, Breteler MM (January 2002). "Prevalence and risk factors of silent brain infarcts in the population-based Rotterdam Scan Study". Stroke. 33 (1): 21–5. doi:10.1161/hs0102.101629. PMID 11779883.
  16. ↑ Kiernan, MC; Vucic, S; Cheah, BC; Turner, MR; Eisen, A; Hardiman, O; Burrell, JR; Zoing, MC (12 March 2011). "Amyotrophic lateral sclerosis". Lancet. 377 (9769): 942–55. doi:10.1016/s0140-6736(10)61156-7. PMID 21296405.
  17. ↑ Belay, Ermias D.; Schonberger, Lawrence B. (1 December 2002). "Variant Creutzfeldt-Jakob disease and bovine spongiform encephalopathy". Clinics in Laboratory Medicine. 22 (4): 849–862, v–vi. doi:10.1016/s0272-2712(02)00024-0. ISSN 0272-2712. PMID 12489284.
  18. ↑ Snowden JS, Neary D, Mann DM; Neary; Mann (February 2002). "Frontotemporal dementia". Br J Psychiatry. 180 (2): 140–3. doi:10.1192/bjp.180.2.140. PMID 11823324.
  19. ↑ Dickson, Dennis; Weller, Roy O. (2011). Neurodegeneration: The Molecular Pathology of Dementia and Movement Disorders (2 ed.). John Wiley & Sons. p. 224. ISBN 9781444341232.
  20. ↑ "Corticobasal Degeneration Information Page: National Institute of Neurological Disorders and Stroke (NINDS)". Retrieved 2009-03-20.
  21. ↑ Goedert, M.; Spillantini, M. G.; Crowther, R. A. (1 July 1991). "Tau proteins and neurofibrillary degeneration". Brain Pathology (Zurich, Switzerland). 1 (4): 279–286. doi:10.1111/j.1750-3639.1991.tb00671.x. ISSN 1015-6305. PMID 1669718.
  22. ↑ Amyloid Deposition as the Central Event in the Aetiology of Alzheimer's Disease. Trends in Pharmacological Sciences. 1991;12(10):383–88. doi:10.1016/0165-6147(91)90609-V. PMID 1763432.
  23. ↑ Galpern, Wendy R.; Lang, Anthony E. (1 March 2006). "Interface between tauopathies and synucleinopathies: a tale of two proteins". Annals of Neurology. 59 (3): 449–458. doi:10.1002/ana.20819. ISSN 0364-5134. PMID 16489609.
  24. ↑ Barranco Quintana, JL; Allam, MF; Del Castillo, AS; Navajas, RF (February 2009). "Parkinson's disease and tea: a quantitative review". Journal of the American College of Nutrition. 28 (1): 1–6. doi:10.1080/07315724.2009.10719754. PMID 19571153.
  25. ↑ Santos C, Costa J, Santos J, Vaz-Carneiro A, Lunet N (2010). "Caffeine intake and dementia: systematic review and meta-analysis". J. Alzheimers Dis. 20 Suppl 1: S187–204. doi:10.3233/JAD-2010-091387. PMID 20182026.
  26. ↑ Marques S, Batalha VL, Lopes LV, Outeiro TF (2011). "Modulating Alzheimer's disease through caffeine: a putative link to epigenetics". J. Alzheimers Dis. 24 (2): 161–71. doi:10.3233/JAD-2011-110032. PMID 21427489.
  27. ↑ Arendash GW, Cao C (2010). "Caffeine and coffee as therapeutics against Alzheimer's disease". J. Alzheimers Dis. 20 Suppl 1: S117–26. doi:10.3233/JAD-2010-091249. PMID 20182037.
  28. ↑ Lourida, Ilianna; Soni, Maya; Thompson-Coon, Joanna; Purandare, Nitin; Lang, Iain A.; Ukoumunne, Obioha C.; Llewellyn, David J. (July 2013). "Mediterranean Diet, Cognitive Function, and Dementia". Epidemiology. 24 (4): 479–489. doi:10.1097/EDE.0b013e3182944410.
  29. ↑ Andrade, Chittaranjan; Radhakrishnan, Rajiv (1 January 2009). "The prevention and treatment of cognitive decline and dementia: An overview of recent research on experimental treatments". Indian Journal of Psychiatry. 51 (1): 12–25. doi:10.4103/0019-5545.44900. ISSN 0019-5545. PMC 2738400. PMID 19742190.
  30. ↑ Farina N, Rusted J, Tabet N (January 2014). "The effect of exercise interventions on cognitive outcome in Alzheimer's disease: a systematic review". Int Psychogeriatr. 26 (1): 9–18. doi:10.1017/S1041610213001385. PMID 23962667.
  31. ↑ Rao AK, Chou A, Bursley B, Smulofsky J, Jezequel J (January 2014). "Systematic review of the effects of exercise on activities of daily living in people with Alzheimer's disease". Am J Occup Ther. 68 (1): 50–56. doi:10.5014/ajot.2014.009035. PMC 5360200. PMID 24367955.
  32. ↑ Mattson MP (2014). "Interventions that improve body and brain bioenergetics for Parkinson's disease risk reduction and therapy". J Parkinsons Dis. 4 (1): 1–13. doi:10.3233/JPD-130335. PMID 24473219.
  33. ↑ Grazina R, Massano J (2013). "Physical exercise and Parkinson's disease: influence on symptoms, disease course and prevention". Rev Neurosci. 24 (2): 139–152. doi:10.1515/revneuro-2012-0087. PMID 23492553.
  34. ↑ van der Kolk NM, King LA (September 2013). "Effects of exercise on mobility in people with Parkinson's disease". Mov. Disord. 28 (11): 1587–1596. doi:10.1002/mds.25658. PMID 24132847.
  35. ↑ Tomlinson CL, Patel S, Meek C, Herd CP, Clarke CE, Stowe R, et al. (September 2013). "Physiotherapy versus placebo or no intervention in Parkinson's disease". Cochrane Database Syst Rev. 9: CD002817. doi:10.1002/14651858.CD002817.pub4. PMID 24018704.
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