Neuroscience of aging: Difference between revisions
Petergstrom (talk | contribs) |
(No difference)
|
Revision as of 04:45, 8 January 2017
The neuroscience of aging is the study of the changes in the nervous system associated with nature Ageing. Aging is associated with many changes in the central nervous system, such as mild atrophy of the cortex that is considered non-pathological. Despite this, aging is also associated with many neurological and neurodegenerative disease such as amyotrophic lateral sclerosis, dementia, mild cognitive impairment, parkinson's disease, and creuzfeldt 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 uncles what the drivers of the change in volume is, however cell death, decreased cell volume, and changes in synaptic structure are all culprits. 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]
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.[6] 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 compensator activation[7] 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.[8]
References
- ^ 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.
- ^ 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.
- ^ 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.
- ^ LeMay, Marjorie (1984). "Radiologic Changes of the Aging Brain and Skull" (PDF). American Journal of Neuroradiology. 5: 269–275.
- ^ 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.
- ^ 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.
- ^ 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.
- ^ 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.