The neurobiology of brain and cognitive reserve: Mental and physical activity as modulators of brain disorders

Nithianantharajah, Jess; Hannan, Anthony J.

doi:10.1016/j.pneurobio.2009.10.001

Cited by 285 publications

(205 citation statements)

References 195 publications

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“…Genetic and early neurodevelopmental factors are still the most important, but not the only, determinant of cognitive reserve. Education, lifestyle and mental and physical activities modify the cognitive reserve through the neuroplasticity of our neural system throughout life (Fratiglioni et al 2004;Roe et al 2007;Nithianantharajah & Hannan, 2009). In patients with schizophrenia, brain reserve and cognitive reserve are low as a consequence abnormal neurodevelopment.…”

Section: Neurodevelopment Cognitive Reserve and Functional Declinementioning

confidence: 99%

Neurodevelopmental origin of cognitive impairment in schizophrenia

2014

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Cognitive impairment is a common feature of schizophrenia; however, its origin remains controversial. Neurodevelopmental abnormalities clearly play a role in pre-morbid cognitive dysfunction in schizophrenia, yet many authors believe that schizophrenia is characterized by illness-related cognitive decline before and after onset of the psychosis that can be the result of neurodegenerative changes. The main reasons behinds such arguments include, first, the evidence showing that effect sizes of the cognitive deficits in subjects who develop adult schizophrenia gradually increase in the first two decades of life and, second, the fact that there is functional decline in many patients with schizophrenia over the years. In this Editorial, I argue that current evidence suggests that illness-related cognitive impairment is neurodevelopmental in origin and characterized by slower gain (developmental lag) but not cognitive decline continuing throughout the first two decades of life. I introduce a model suggesting that neurodevelopmental abnormality can in fact explain the course of cognitive dysfunction and variations in the trajectory of functional decline throughout the life in individuals with schizophrenia. In this model, the severity of underlying neurodevelopmental abnormality determines the age that cognitive deficits first become apparent and contributes to the cognitive reserve of the individual. Interaction of neurodevelopmental abnormality with clinical symptoms, especially negative symptoms and aging, vascular changes, psychological and iatrogenic factors contributes to the heterogeneity of the functional trajectory observed in this disorder.

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Section: Neurodevelopment Cognitive Reserve and Functional Declinementioning

confidence: 99%

Neurodevelopmental origin of cognitive impairment in schizophrenia

2014

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“…Enriched environment (EE) is an experimental paradigm defined as "a combination of complex and inanimate social stimulation" [17] that induces cellular, molecular and behavioural effects, not only in standard conditions but also in pathological ones [18,19]. Whereas initial studies showed that EE modified cortical weight [20,21], subsequent studies described an increase of nuclear and soma size in neurons, dendritic branching or synapsis size [22][23][24] among other effects.…”

Section: Introductionmentioning

confidence: 99%

VEGF reverts the cognitive impairment induced by a focal traumatic brain injury during the development of rats raised under environmental enrichment

Ortuzar

Rico‐Barrio

Bengoetxea

et al. 2013

Behavioural Brain Research

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The role of VEGF in the nervous system is extensive; apart from its angiogenic effect, VEGF has been described as a neuroprotective, neurotrophic and neurogenic molecule. Similar effects have been described for enriched environment (EE). Moreover, both VEGF and EE have been related to improved spatial memory. Our aim was to investigate the neurovascular and cognitive effects of intracerebrallyadministered VEGF and enriched environment during the critical period of the rat visual cortex development. Results showed that VEGF infusion as well as enriched environment induced neurovascular and cognitive effects in developing rats. VEGF administration produced an enhancement during the learning process of enriched animals and acted as an angiogenic factor both in primary visual cortex (V1) and dentate gyrus (DG) in order to counteract minipump implantation-induced damage. This fact revealed that DG vascularization is critical for normal learning. In contrast to this enriched environment acted on the neuronal density of the DG and V1 cortex, and results showed learning enhancement only in non-operated rats. In conclusion, VEGF administration only has effects if damage is observed due to injury. Once control values were reached, no further effects appeared, showing a ceiling effect. Our results strongly support that in addition to neurogenesis, vascularization plays a pivotal role for learning and memory.

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“…These paradigms influence neural plasticity (Cordoba et al, 1984;García-Segura, 2009;Nithianantharajah and Hannan, 2009;Petrosini et al, 2009;Sale et al, 2009) and synaptic plasticity (Christie et al, 2008), inducing changes in the rate of adult hippocampal neurogenesis (Kempermann et al, 1997b). Moreover, in the long-term, such activity has a direct impact on the ability to cope with life events, known as animal's cognitive reserve (Mandolesi et al, 2008;Milgram et al, 2006) and neurogenic reserve (Kempermann, 2008), respectively.…”

Section: Introductionmentioning

confidence: 99%

Antidepressant and Proneurogenic Influence of Environmental Enrichment in Mice: Protective Effects vs Recovery

Llorens‐Martin

Tejeda

Trejo

2011

Neuropsychopharmacol

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Physical-cognitive activity has long-lasting beneficial effects on the brain and on behavior. Environmental enrichment (EE) induces brain activity known to influence the behavior of mice, as measured in learned helplessness paradigms (forced swim test), and neurogenic cell populations in the hippocampal dentate gyrus. However, it is not completely clear whether the antidepressant and proneurogenic effects of EE are different in animals that are naive or pre-exposed to the stress inducing helplessness, and if this depends on the type of stressor. It also remains unclear whether differential effects are exerted on distinct neurogenic subpopulations. We found that EE has a protective effect in adult female mice (C57BL/6J) when exposed twice to the same stressor (forced swim test) but it has no influence on recovery. The repeated exposure to this stressor was analyzed together with the effects of EE on different neurogenic populations distinguished by age and differentiation state. Younger cells are more sensitive and responsive to the conditions, both the positive and negative effects. These results are relevant to identify the cell populations that are the targets of stress, depression, and enrichment, and that form part of the mechanism responsible for mood dysfunctions.

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The neurobiology of brain and cognitive reserve: Mental and physical activity as modulators of brain disorders

Cited by 285 publications

References 195 publications

Neurodevelopmental origin of cognitive impairment in schizophrenia

Neurodevelopmental origin of cognitive impairment in schizophrenia

VEGF reverts the cognitive impairment induced by a focal traumatic brain injury during the development of rats raised under environmental enrichment

Antidepressant and Proneurogenic Influence of Environmental Enrichment in Mice: Protective Effects vs Recovery

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