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Environmental enrichment (neural)

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File:Rat coming out cage.jpg

A rodent is not stimulated by the environment in a wire cage, and this affects its brain negatively, particularly the complexity of its synaptic connections

Environmental enrichment concerns how the brain is affected by the stimulation of its information processing provided by its surroundings (including the opportunity to interact socially). Brains in richer, more stimulating environments, have increased numbers of synapses, and the dendrite arbors upon which they reside are more complex. This effect happens particularly during neurodevelopment, but also to a lesser degree in adulthood. With extra synapses there is also increased synapse activity and so increased size and number of glial energy support cells. Capillary vasculation also is greater to provide the neurons and glial cells with extra energy. The neuropil (neurons, glial cells, capillaries, combined together) expands making the cortex thicker. There may also exist (at least in rodents) more neurons.

Research in nonhuman animals finds that more stimulating environment could aid the treatment and recovery of a diverse variety of brain related dysfunctions, including Alzheimer’s disease and those connected to aging, whereas a lack of stimulation might impair cognitive development.

Research upon humans suggests that lack of stimulation (deprivation—such as in old-style orphanages) delays and impairs cognitive development. Research also finds that higher levels of education (which is both cognitively stimulating in itself, and associates with people engaging in more challenging cognitive activities) results in greater resilience (cognitive reserve) to the effects of aging and dementia.

Early research[]

Donald O. Hebb in 1947 found that rats raised as pets performed better on problem solving tests than rats raised in cages.[1] His research, however, did not investigate the brain nor use standardized impoverished and enriched environments. Research doing this first was started in 1960 by Mark Rosenzweig who compared single rats in normal cages, and those placed in ones with toys, ladders, tunnels, running wheels in groups. This found that growing up in enriched environents affected enzyme cholinesterase activity.[2] This work led in 1962 to the discovery that environmental enrichment increased cerebral cortex volume.[3] In 1964, it was found that this was due to increased cerebral cortex thickness and greater synapse and glial numbers.[4][5]

Also starting around 1960, Harry Harlow studied the effects of maternal and social deprivation on rhesus monkey infants (a form of environmental stimulus deprivation). This established the importance of social stimulation for normal cognitive and emotional development.[6]

Synapses[]

Synaptogenesis[]

Rats raised with environmental enrichment have thicker cerebral cortices (3.3-7%) that contain 25% more synapses.[5][7] This effect of environmental richness upon the brain occurs whether it is experienced immediately following birth,[8] after weaning,[5][7][9] or during maturity.[10] When synapse numbers increase in adults, they can remain high in number even when the adults are returned to improvised environment for 30 days[10] suggesting that such increases in synapse numbers are not necessarily temporary. However, the increase in synapse numbers has been observed generally to reduce with maturation.[11][12] Stimulation affects not only synapses upon pyramidal neurons (the main projecting neurons in the cerebral cortex) but also stellate ones (that are usually interneurons).[13] It also can affect neurons outside the brain in the retina.[14]

Dendrite complexity[]

Environmental enrichment affects the complexity and length of the dendrite arbors (upon which synapses form). Higher-order dendrite branch complexity is increased in enriched environments,[13][15] as can the length, in young animals, of distal branches.[16]

Activity and energy consumption[]

Synapses in animals in enriched environments show evidence of increased synapse activation.[17] Synapses tend to also be much larger.[18] This increased energy consumption is reflected in glial and local capillary vasculation that provides synapses with extra energy.

  • Glial cell numbers per neuron increase 12-14%[5][7]
  • The direct apposition area of glial cells with synapses expands by 19%[19]
  • The volume of glial cell nuclei for each synapse is higher by 37.5%[17]
  • The mean volume of mitochondria per neuron is 20% greater[17]
  • The volume of glial cell nuclei for each neuron is 63% higher[17]
  • Capillary density is increased.[20]
  • Capillaries are wider (4.35 μm compared to 4.15 μm in controls) [17]
  • Shorter distance exist between any part of the neuropil and a capillary (27.6 μm compared to 34.6 μm)[17]

These energy related changes to the neuropil are responsible for increasing the volume of the cerebral cortex (the increase in synapse numbers contributes in itself hardly any extra volume).

Motor learning stimulation[]

Part of the effect of environmental enrichment is providing opportunities to acquire motor skills. Research upon “acrobatic” skill learning in the rat shows that it leads to increased synapse numbers.[21][22]

Maternal transmission[]

Environmental enrichment during pregnancy has effects upon the fetus such as accelerating its retinal development.[23]

Neurogenesis[]

Environmental enrichment can also lead to the formation of neurons (at least in rats)[24] and reverses the loss of neurons in the hippocampus and memory impairment following chronic stress.[25] However, its relevance has been questioned for the behavioral effects of enriched environments.[26]

Mechanisms[]

Enriched environments affect the expression of genes in the cerebral cortex and the hippocampus that determine neuronal structure.[27] At the molecular level, this occurs through increased concentrations of the neurotrophins NGF, NT-3,[28][29] and changes in BDNF.[14][30] This alters the activation of cholinergic neurons,[29] 5-HT,[31] and beta-adrenolin.[32] Another effect is to increase proteins such as synaptophysin and PSD-95 in synapses.[33] Changes in Wnt signaling have also been found to mimic in adult mice the effects of environmental enrichment upon synapses in the hippocampus.[34] Increase in neurons numbers could be linked to changes in VEGF.[35]

Resilience and rehabilitation[]

Research (as least upon rats) suggests that environment enrichment might reduce the effects or ameliorate the cognitive impairments caused by a diverse variety of conditions and neurological disorders.

Humans[]

Though environmental enrichment research has been mostly done upon rodents, similar effects occur in primates,[58] and are likely to affect the human brain. However, direct research upon human synapses and their numbers is limited since this requires histological study of the brain. A link, however, has been found between educational level and greater dendritic branch complexity following autopsy removal of the brain.[59]

Localized cerebral cortex changes[]

MRI detects localized cerebral cortex expansion after people learn complex tasks such as mirror reading (in this case in the right occipital cortex),[60] three-ball juggling (bilateral mid-temporal area and left posterior intraparietal sulcus),[61] and when medical students intensively revise for exams (bilaterally in the posterior and lateral parietal cortex).[62] Such changes in gray matter volume can be expected to link to changes in synapse numbers due to the increased numbers of glial cells and the expanded capillary vascularization needed to support their increased energy consumption.

Institutional deprivation[]

Children that receive impoverished stimulation due to being confined to cots without social interaction or reliable caretakers in low quality orphanages show severe delays in cognitive and social development.[63] 12% of them if adopted after 6 months of age show autistic or mildly autistic traits later at four years of age.[64] Some children in such impoverished orphanages at two and half years of age still fail to produce intelligible words, though a year of foster care enabled such children to catch up in their language in most respects.[65] Catch-up in other cognitive functioning also occurs after adoption, though problems continue in many children if this happens after the age of 6 months[66]

Such children show marked differences in their brains, consistent with research upon experiment animals, compared to children from normally stimulating environments. They have reduced brain activity in the orbital prefrontal cortex, amygdala, hippocampus, temporal cortex, and brain stem.[67] They also showed less developed white matter connections between different areas in their cerebral cortices, particularly the uncinate fasciculus.[68]

Conversely, enriching the experience of preterm infants with massage quickens the maturating of their electroencephalographic activity and their visual acuity. Moreover, as with enrichment in experimental animals, this associates with an increase in IGF-1.[69]

Cognitive reserve and resilience[]

Another source of evidence for the effect of environment stimulation upon the human brain is cognitive reserve (a measure of the brain’s resilience to cognitive impairment) and the level of a person’s education. Not only is higher education linked to a more cognitively demanding educational experience, but it also correlates with a person’s generally engaging in cognitively demanding activities.[70] The more education a person has received, the less the effects of aging,[71][72] dementia,[73] white matter hyperintensities,[74] MRI-defined brain infarcts,[75] Alzheimer’s disease,[76][77] and traumatic brain injury.[78] Also, aging and dementia are less in those that engage in complex cognitive tasks.[79] The cognitive decline of those with epilepsy could also be affected by the level of a person’s education.[80]

See also[]

Notes[]

  1. ↑ Hebb DO (1947). The effects of early experience on problem solving at maturity. American Psychologist 2: 306–7.
  2. ↑ Krech D, Rosenzweig MR, Bennett EL (December 1960). Effects of environmental complexity and training on brain chemistry. J Comp Physiol Psychol 53: 509–19.
  3. ↑ Rosenzweig MR, Krech D, Bennett EL, Diamond MC (August 1962). Effects of environmental complexity and training on brain chemistry and anatomy: a replication and extension. J Comp Physiol Psychol 55: 429–37.
  4. ↑ Altman J, Das GD (December 1964). Autoradiographic Examination of the Effects of Enriched Environment on the Rate of Glial Multiplication in the Adult Rat Brain. Nature 204 (4964): 1161–3.
  5. ↑ 5.0 5.1 5.2 5.3 Diamond MC, Krech D, Rosenzweig MR (August 1964). The Effects of an Enriched Environment on the Histology of the Rat Cerebral Cortex. J. Comp. Neurol. 123: 111–20.
  6. ↑ Harlow HF, Rowland GL, Griffin GA (December 1964). The Effect of Total Social Deprivation on the Development of Monkey Behavior. Psychiatr Res Rep Am Psychiatr Assoc 19: 116–35.
  7. ↑ 7.0 7.1 7.2 Diamond MC, Law F, Rhodes H, et al. (September 1966). Increases in cortical depth and glia numbers in rats subjected to enriched environment. J. Comp. Neurol. 128 (1): 117–26.
  8. ↑ Schapiro S, Vukovich KR (January 1970). Early experience effects upon cortical dendrites: a proposed model for development. Science 167 (3916): 292–4.
  9. ↑ Bennett EL, Diamond MC, Krech D, Rosenzweig MR (October 1964). Chemical and Anatomical Plasticity Brain. Science 146 (3644): 610–9.
  10. ↑ 10.0 10.1 Briones TL, Klintsova AY, Greenough WT (August 2004). Stability of synaptic plasticity in the adult rat visual cortex induced by complex environment exposure. Brain Res. 1018 (1): 130–5.
  11. ↑ Holtmaat AJ, Trachtenberg JT, Wilbrecht L, et al. (January 2005). Transient and persistent dendritic spines in the neocortex in vivo. Neuron 45 (2): 279–91.
  12. ↑ Zuo Y, Lin A, Chang P, Gan WB (April 2005). Development of long-term dendritic spine stability in diverse regions of cerebral cortex. Neuron 46 (2): 181–9.
  13. ↑ 13.0 13.1 Greenough WT, Volkmar FR (August 1973). Pattern of dendritic branching in occipital cortex of rats reared in complex environments. Exp. Neurol. 40 (2): 491–504.
  14. ↑ 14.0 14.1 Landi S, Sale A, Berardi N, Viegi A, Maffei L, Cenni MC (January 2007). Retinal functional development is sensitive to environmental enrichment: a role for BDNF. FASEB J. 21 (1): 130–9.
  15. ↑ Volkmar FR, Greenough WT (June 1972). Rearing complexity affects branching of dendrites in the visual cortex of the rat. Science 176 (4042): 1445–7.
  16. ↑ Wallace CS, Kilman VL, Withers GS, Greenough WT (July 1992). Increases in dendritic length in occipital cortex after 4 days of differential housing in weanling rats. Behav. Neural Biol. 58 (1): 64–8.
  17. ↑ 17.0 17.1 17.2 17.3 17.4 17.5 Sirevaag AM, Greenough WT (October 1987). Differential rearing effects on rat visual cortex synapses. III. Neuronal and glial nuclei, boutons, dendrites, and capillaries. Brain Res. 424 (2): 320–32.
  18. ↑ Sirevaag AM, Greenough WT (April 1985). Differential rearing effects on rat visual cortex synapses. II. Synaptic morphometry. Brain Res. 351 (2): 215–26.
  19. ↑ Jones TA, Greenough WT (January 1996). Ultrastructural evidence for increased contact between astrocytes and synapses in rats reared in a complex environment. Neurobiol Learn Mem 65 (1): 48–56.
  20. ↑ Borowsky IW, Collins RC (October 1989). Metabolic anatomy of brain: a comparison of regional capillary density, glucose metabolism, and enzyme activities. J. Comp. Neurol. 288 (3): 401–13.
  21. ↑ Black JE, Isaacs KR, Anderson BJ, Alcantara AA, Greenough WT (July 1990). Learning causes synaptogenesis, whereas motor activity causes angiogenesis, in cerebellar cortex of adult rats. Proc. Natl. Acad. Sci. U.S.A. 87 (14): 5568–72.
  22. ↑ Kleim JA, Hogg TM, VandenBerg PM, Cooper NR, Bruneau R, Remple M (January 2004). Cortical synaptogenesis and motor map reorganization occur during late, but not early, phase of motor skill learning. J. Neurosci. 24 (3): 628–33.
  23. ↑ Sale A, Cenni MC, Ciucci F, Putignano E, Chierzi S, Maffei L (2007). Maternal enrichment during pregnancy accelerates retinal development of the fetus. PLoS ONE 2 (11): e1160.
  24. ↑ Fan Y, Liu Z, Weinstein PR, Fike JR, Liu J (January 2007). Environmental enrichment enhances neurogenesis and improves functional outcome after cranial irradiation. Eur. J. Neurosci. 25 (1): 38–46.
  25. ↑ Veena J, Srikumar BN, Mahati K, Bhagya V, Raju TR, Shankaranarayana Rao BS (March 2009). Enriched environment restores hippocampal cell proliferation and ameliorates cognitive deficits in chronically stressed rats. J. Neurosci. Res. 87 (4): 831–43.
  26. ↑ Meshi D, Drew MR, Saxe M, et al. (June 2006). Hippocampal neurogenesis is not required for behavioral effects of environmental enrichment. Nat. Neurosci. 9 (6): 729–31.
  27. ↑ Rampon C, Jiang CH, Dong H, et al. (November 2000). Effects of environmental enrichment on gene expression in the brain. Proc. Natl. Acad. Sci. U.S.A. 97 (23): 12880–4.
  28. ↑ Ickes BR, Pham TM, Sanders LA, Albeck DS, Mohammed AH, Granholm AC (July 2000). Long-term environmental enrichment leads to regional increases in neurotrophin levels in rat brain. Exp. Neurol. 164 (1): 45–52.
  29. ↑ 29.0 29.1 Torasdotter M, Metsis M, Henriksson BG, Winblad B, Mohammed AH (June 1998). Environmental enrichment results in higher levels of nerve growth factor mRNA in the rat visual cortex and hippocampus. Behav. Brain Res. 93 (1-2): 83–90.
  30. ↑ Zhu SW, Codita A, Bogdanovic N, et al. (February 2009). Influence of environmental manipulation on exploratory behaviour in male BDNF knockout mice. Behav. Brain Res. 197 (2): 339–46.
  31. ↑ Rasmuson S, Olsson T, Henriksson BG, et al. (January 1998). Environmental enrichment selectively increases 5-HT1A receptor mRNA expression and binding in the rat hippocampus. Brain Res. Mol. Brain Res. 53 (1-2): 285–90.
  32. ↑ Escorihuela RM, Fernández-Teruel A, Tobeña A, et al. (July 1995). Early environmental stimulation produces long-lasting changes on beta-adrenoceptor transduction system. Neurobiol Learn Mem 64 (1): 49–57.
  33. ↑ Nithianantharajah J, Levis H, Murphy M (May 2004). Environmental enrichment results in cortical and subcortical changes in levels of synaptophysin and PSD-95 proteins. Neurobiol Learn Mem 81 (3): 200–10.
  34. ↑ Gogolla N, Galimberti I, Deguchi Y, Caroni P (May 2009). Wnt signaling mediates experience-related regulation of synapse numbers and mossy fiber connectivities in the adult hippocampus. Neuron 62 (4): 510–25.
  35. ↑ During MJ, Cao L (February 2006). VEGF, a mediator of the effect of experience on hippocampal neurogenesis. Curr Alzheimer Res 3 (1): 29–33.
  36. ↑ Mattson MP, Duan W, Lee J, Guo Z (May 2001). Suppression of brain aging and neurodegenerative disorders by dietary restriction and environmental enrichment: molecular mechanisms. Mech. Ageing Dev. 122 (7): 757–78.
  37. ↑ Milgram NW, Siwak-Tapp CT, Araujo J, Head E (August 2006). Neuroprotective effects of cognitive enrichment. Ageing Res. Rev. 5 (3): 354–69.
  38. ↑ Berardi N, Braschi C, Capsoni S, Cattaneo A, Maffei L (June 2007). Environmental enrichment delays the onset of memory deficits and reduces neuropathological hallmarks in a mouse model of Alzheimer-like neurodegeneration. J. Alzheimers Dis. 11 (3): 359–70.
  39. ↑ Spires TL, Grote HE, Varshney NK, et al. (March 2004). Environmental enrichment rescues protein deficits in a mouse model of Huntington's disease, indicating a possible disease mechanism. J. Neurosci. 24 (9): 2270–6.
  40. ↑ Faherty CJ, Raviie Shepherd K, Herasimtschuk A, Smeyne RJ (March 2005). Environmental enrichment in adulthood eliminates neuronal death in experimental Parkinsonism. Brain Res. Mol. Brain Res. 134 (1): 170–9.
  41. ↑ Johansson BB (February 1996). Functional outcome in rats transferred to an enriched environment 15 days after focal brain ischemia. Stroke 27 (2): 324–6.
  42. ↑ Fischer FR, Peduzzi JD (2007). Functional recovery in rats with chronic spinal cord injuries after exposure to an enriched environment. J Spinal Cord Med 30 (2): 147–55.
  43. ↑ Sale A, Maya Vetencourt JF, Medini P, et al. (June 2007). Environmental enrichment in adulthood promotes amblyopia recovery through a reduction of intracortical inhibition. Nat. Neurosci. 10 (6): 679–81.
  44. ↑ Kondo M, Gray LJ, Pelka GJ, Christodoulou J, Tam PP, Hannan AJ (June 2008). Environmental enrichment ameliorates a motor coordination deficit in a mouse model of Rett syndrome--Mecp2 gene dosage effects and BDNF expression. Eur. J. Neurosci. 27 (12): 3342–50.
  45. ↑ Schneider T, Turczak J, Przewłocki R (January 2006). Environmental enrichment reverses behavioral alterations in rats prenatally exposed to valproic acid: issues for a therapeutic approach in autism. Neuropsychopharmacology 31 (1): 36–46.
  46. ↑ Magalhães A, Melo P, Alves CJ, Tavares MA, de Sousa L, Summavielle T (October 2008). Exploratory behavior in rats postnatally exposed to cocaine and housed in an enriched environment. Ann. N. Y. Acad. Sci. 1139: 358–65.
  47. ↑ Solinas M, Chauvet C, Thiriet N, El Rawas R, Jaber M (November 2008). Reversal of cocaine addiction by environmental enrichment. Proc. Natl. Acad. Sci. U.S.A. 105 (44): 17145–50.
  48. ↑ Solinas M, Thiriet N, El Rawas R, Lardeux V, Jaber M (April 2009). Environmental enrichment during early stages of life reduces the behavioral, neurochemical, and molecular effects of cocaine. Neuropsychopharmacology 34 (5): 1102–11.
  49. ↑ Hannigan JH, Berman RF (2000). Amelioration of fetal alcohol-related neurodevelopmental disorders in rats: exploring pharmacological and environmental treatments. Neurotoxicol Teratol 22 (1): 103–11.
  50. ↑ Hannigan JH, O'leary-Moore SK, Berman RF (2007). Postnatal environmental or experiential amelioration of neurobehavioral effects of perinatal alcohol exposure in rats. Neurosci Biobehav Rev 31 (2): 202–11.
  51. ↑ Cao X, Huang S, Ruan D (April 2008). Enriched environment restores impaired hippocampal long-term potentiation and water maze performance induced by developmental lead exposure in rats. Dev Psychobiol 50 (3): 307–13.
  52. ↑ Guilarte TR, Toscano CD, McGlothan JL, Weaver SA (January 2003). Environmental enrichment reverses cognitive and molecular deficits induced by developmental lead exposure. Ann. Neurol. 53 (1): 50–6.
  53. ↑ Abrahám IM, Kovács KJ (August 2000). Postnatal handling alters the activation of stress-related neuronal circuitries. Eur. J. Neurosci. 12 (8): 3003–14.
  54. ↑ Francis DD, Diorio J, Plotsky PM, Meaney MJ (September 2002). Environmental enrichment reverses the effects of maternal separation on stress reactivity. J. Neurosci. 22 (18): 7840–3.
  55. ↑ Leal-Galicia P, Saldívar-González A, Morimoto S, Arias C (March 2007). Exposure to environmental enrichment elicits differential hippocampal cell proliferation: role of individual responsiveness to anxiety. Dev Neurobiol 67 (4): 395–405.
  56. ↑ Bredy TW, Humpartzoomian RA, Cain DP, Meaney MJ (2003). Partial reversal of the effect of maternal care on cognitive function through environmental enrichment. Neuroscience 118 (2): 571–6.
  57. ↑ Argandoña EG, Bengoetxea H, Lafuente JV. (2009). Physical exercise is required for environmental enrichment to offset the quantitative effects of dark-rearing on the S-100β astrocytic density in the rat visual cortex. Journal of Anatomy 215 (2): 132–140.
  58. ↑ Kozorovitskiy Y, Gross CG, Kopil C, et al. (November 2005). Experience induces structural and biochemical changes in the adult primate brain. Proc. Natl. Acad. Sci. U.S.A. 102 (48): 17478–82.
  59. ↑ Jacobs B, Schall M, Scheibel AB (January 1993). A quantitative dendritic analysis of Wernicke's area in humans. II. Gender, hemispheric, and environmental factors. J. Comp. Neurol. 327 (1): 97–111.
  60. ↑ Ilg R, Wohlschläger AM, Gaser C, et al. (April 2008). Gray matter increase induced by practice correlates with task-specific activation: a combined functional and morphometric magnetic resonance imaging study. J. Neurosci. 28 (16): 4210–5.
  61. ↑ Draganski B, Gaser C, Busch V, Schuierer G, Bogdahn U, May A (January 2004). Neuroplasticity: changes in grey matter induced by training. Nature 427 (6972): 311–2.
  62. ↑ Draganski B, Gaser C, Kempermann G, et al. (June 2006). Temporal and spatial dynamics of brain structure changes during extensive learning. J. Neurosci. 26 (23): 6314–7.
  63. ↑ Kaler SR, Freeman BJ (May 1994). Analysis of environmental deprivation: cognitive and social development in Romanian orphans. J Child Psychol Psychiatry 35 (4): 769–81.
  64. ↑ Rutter M, Andersen-Wood L, Beckett C, et al. (May 1999). Quasi-autistic patterns following severe early global privation. English and Romanian Adoptees (ERA) Study Team. J Child Psychol Psychiatry 40 (4): 537–49.
  65. ↑ Windsor J, Glaze LE, Koga SF (October 2007). Language acquisition with limited input: Romanian institution and foster care. J. Speech Lang. Hear. Res. 50 (5): 1365–81.
  66. ↑ Beckett C, Maughan B, Rutter M, et al. (2006). Do the effects of early severe deprivation on cognition persist into early adolescence? Findings from the English and Romanian adoptees study. Child Dev 77 (3): 696–711.
  67. ↑ Chugani HT, Behen ME, Muzik O, Juhász C, Nagy F, Chugani DC (December 2001). Local brain functional activity following early deprivation: a study of postinstitutionalized Romanian orphans. Neuroimage 14 (6): 1290–301.
  68. ↑ Eluvathingal TJ, Chugani HT, Behen ME, et al. (June 2006). Abnormal brain connectivity in children after early severe socioemotional deprivation: a diffusion tensor imaging study. Pediatrics 117 (6): 2093–100.
  69. ↑ Guzzetta A, Baldini S, Bancale A, et al. (May 2009). Massage accelerates brain development and the maturation of visual function. J. Neurosci. 29 (18): 6042–51.
  70. ↑ Wilson R, Barnes L, Bennett D (August 2003). Assessment of lifetime participation in cognitively stimulating activities. J Clin Exp Neuropsychol 25 (5): 634–42.
  71. ↑ Corral M, Rodríguez M, Amenedo E, Sánchez JL, Díaz F (2006). Cognitive reserve, age, and neuropsychological performance in healthy participants. Dev Neuropsychol 29 (3): 479–91.
  72. ↑ Fritsch T, McClendon MJ, Smyth KA, Lerner AJ, Friedland RP, Larsen JD (June 2007). Cognitive functioning in healthy aging: the role of reserve and lifestyle factors early in life. Gerontologist 47 (3): 307–22.
  73. ↑ Hall CB, Derby C, LeValley A, Katz MJ, Verghese J, Lipton RB (October 2007). Education delays accelerated decline on a memory test in persons who develop dementia. Neurology 69 (17): 1657–64.
  74. ↑ Nebes RD, Meltzer CC, Whyte EM, et al. (2006). The relation of white matter hyperintensities to cognitive performance in the normal old: education matters. Neuropsychol Dev Cogn B Aging Neuropsychol Cogn 13 (3-4): 326–40.
  75. ↑ Elkins JS, Longstreth WT, Manolio TA, Newman AB, Bhadelia RA, Johnston SC (August 2006). Education and the cognitive decline associated with MRI-defined brain infarct. Neurology 67 (3): 435–40.
  76. ↑ Koepsell TD, Kurland BF, Harel O, Johnson EA, Zhou XH, Kukull WA (May 2008). Education, cognitive function, and severity of neuropathology in Alzheimer disease. Neurology 70 (19 Pt 2): 1732–9.
  77. ↑ Roe CM, Mintun MA, D'Angelo G, Xiong C, Grant EA, Morris JC (November 2008). Alzheimer disease and cognitive reserve: variation of education effect with carbon 11-labeled Pittsburgh Compound B uptake. Arch. Neurol. 65 (11): 1467–71.
  78. ↑ Kesler SR, Adams HF, Blasey CM, Bigler ED (2003). Premorbid intellectual functioning, education, and brain size in traumatic brain injury: an investigation of the cognitive reserve hypothesis. Appl Neuropsychol 10 (3): 153–62.
  79. ↑ Fratiglioni L, Paillard-Borg S, Winblad B (June 2004). An active and socially integrated lifestyle in late life might protect against dementia. Lancet Neurol 3 (6): 343–53.
  80. ↑ Pai MC, Tsai JJ (2005). Is cognitive reserve applicable to epilepsy? The effect of educational level on the cognitive decline after onset of epilepsy. Epilepsia 46 (Suppl 1): 7–10.

Bibliography[]

  • Diamond, Marian Cleeves (1988). Enriching heredity: the impact of the environment on the anatomy of the brain, New York: Free Press.
  • Jensen, Eric (2006). Enriching the brain: how to maximize every learner's potential, San Francisco: Jossey-Bass, A John Wiley & Sons Imprint.
  • Renner, M. J. Rosenzweig, M. R. (1987). Enriched and Impoverished Environments: Effects on Brain and Behavior, New York: Springer-Verlag.

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