Neuroscience
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Brain plasticity is the ability of the nervous system to change structurally and functionally in response to experience. By shaping brain structure and function, experience leads to the creation of a protective reserve that accounts for differences among individuals in susceptibility to age-related brain modifications and pathology. This review is aimed to address the biological bases of the experience-dependent "brain reserve" by describing the results of animal studies that focused on the neuroanatomical and molecular effects of environmental enrichment. ⋯ On the whole, studies of the structural and molecular effects of environmental enrichment strongly support the neuroprotective action of a particularly stimulating lifestyle on cognitive functions. Our current level of understanding of these effects and mechanisms is such that additional and novel studies, systematic reviews, and meta-analyses are necessary to investigate the specific effects of the different components of environmental enrichment in both healthy and pathological models. Only in this way can comprehensive recommendations for proper life habits be developed.
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Neuroimaging epigenetics is an interdisciplinary application of epigenetics to cognitive neuroscience that seeks to identify molecular and neural predictors of human behavior. This approach can be sensitive to the dynamic interaction between biological predisposition and environmental influences, and is potentially more informative than an approach using static genetic code. Recent work in this field has generated considerable enthusiasm, yet caution is warranted since any novel cross-disciplinary approach lacks a set of established conventions or standards. In this paper we review existing research in the field of imaging epigenetics, outline important caveats and considerations, and suggest a set of guidelines for researchers conducting this work.
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Social neuroscience, the study of the neurobiological basis of social behavior, has become a major area of current research in behavioral neuroscience and psychiatry, since many psychiatric disorders are characterized by social deficits. Social behavior refers to the behavioral response with regard to socially relevant information, and requires the perception and integration of social cues through a complex cognition process (i.e. social cognition) that involves attention, memory, motivation and emotion. Neurobiological and molecular mechanisms underlying social behavior are highly conserved across species, and inter- and intra-specific variability observed in social behavior can be explained to large extent by differential activity of this conserved neural network. ⋯ Thus, quantitative variation in the levels, release and/or receptor density of these molecules could affect the observed behavioral response. The present review presents an overall framework of the components of the social brain circuitry and its modulation. By integrating multiple research approaches, from human fMRI studies to animal models we can start shedding light into how dysfunction in these circuits could lead to disorders of social-functioning such as Autism.
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Mitochondria densely populate cells in central nervous system providing essential energy for neurons and influencing synaptic plasticity. Harm to these organelles can impair cognitive performance through damaged neurotransmission and altered Ca2+ homeostasis. Impaired cognition could be one underlying factor which can characterize major depressive disorder, a huge burden for society marked by depressed mood and anhedonia. ⋯ Since several different biological and environmental factors can lead to depression, mitochondrial changes may represent a significant subgroup of depressive patients although cognitive correlates can remain undiscovered without a specific focus. Hypothesis driven studies instead of GWAS can pinpoint targets relevant only in a subset of depressed population. This review highlights results mainly from candidate gene studies on nuclear DNA of mitochondrion-related proteins, including TOMM40, MTHFD1L, ATP6V1B2 and MAO genes, also implicated in Alzheimer's disease, and alterations in the mitochondrial genome to argue for endophenotypes where impaired mitochondrial function may be the leading cause for depressive symptomatology and parallel cognitive dysfunction.