Neuroscience and biobehavioral reviews
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Memory loss is the key symptom of dementia-related disorders, including the prevalent Alzheimer's disease (AD). To date, pharmacological treatments for AD have limited and short-lasting effects. Therefore, researchers are investigating novel therapies such as deep brain stimulation (DBS) to treat memory impairment and to reduce or stop the progression of it. ⋯ The mechanisms underlying memory enhancement may include the release of specific neurotransmitters and neuroplasticity. Some authors suggest that DBS might even be disease-modifying. Nevertheless, it is still premature to conclude that DBS can be used in the treatment of AD, and the field will wait for the results of ongoing clinical trials.
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Neurosci Biobehav Rev · Dec 2013
ReviewCognitive unbinding: a neuroscientific paradigm of general anesthesia and related states of unconsciousness.
"Cognitive unbinding" refers to the impaired synthesis of specialized cognitive activities in the brain and has been proposed as a mechanistic paradigm of unconsciousness. This article draws on recent neuroscientific data to revisit the tenets and predictions of cognitive unbinding, using general anesthesia as a representative state of unconsciousness. ⋯ The relevance of cognitive unbinding to sleep, disorders of consciousness, and psychological processes is also explored. It is concluded that cognitive unbinding is a viable neuroscientific framework for unconscious processes across the fields of anesthesiology, sleep neurobiology, neurology and psychoanalysis.
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Neurosci Biobehav Rev · Nov 2013
ReviewBeneficial effects of physical exercise on neuroplasticity and cognition.
The human brain adapts to changing demands by altering its functional and structural properties ("neuroplasticity") which results in learning and acquiring skills. Convergent evidence from both human and animal studies suggests that physical activity facilitates neuroplasticity of certain brain structures and as a result cognitive functions. Animal studies have identified an enhancement of neurogenesis, synaptogenesis, angiogenesis and the release of neurotrophins as neural mechanisms mediating beneficial cognitive effects of physical exercise. ⋯ The results suggest that physical exercise may trigger processes facilitating neuroplasticity and, thereby, enhances an individual's capacity to respond to new demands with behavioral adaptations. Indeed, some recent studies have suggested that combining physical and cognitive training might result in a mutual enhancement of both interventions. Moreover, new data suggest that to maintain the neuro-cognitive benefits induced by physical exercise, an increase in the cardiovascular fitness level must be maintained.
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Neurosci Biobehav Rev · Sep 2013
ReviewAscending monoaminergic systems alterations in Alzheimer's disease. translating basic science into clinical care.
Extensive neuropathological studies have established a compelling link between abnormalities in structure and function of subcortical monoaminergic (MA-ergic) systems and the pathophysiology of Alzheimer's disease (AD). The main cell populations of these systems including the locus coeruleus, the raphe nuclei, and the tuberomamillary nucleus undergo significant degeneration in AD, thereby depriving the hippocampal and cortical neurons from their critical modulatory influence. ⋯ This review aims to explore the link between abnormalities in the MA-ergic systems and AD symptomatology as well as the therapeutic strategies targeting these systems. Furthermore, we will examine possible mechanisms behind basic vulnerability of MA-ergic neurons in AD.
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Neurosci Biobehav Rev · Sep 2013
ReviewEffects of diabetes on hippocampal neurogenesis: links to cognition and depression.
Diabetes often leads to a number of complications involving brain function, including cognitive decline and depression. In addition, depression is a risk factor for developing diabetes. A loss of hippocampal neuroplasticity, which impairs the ability of the brain to adapt and reorganize key behavioral and emotional functions, provides a framework for understanding this reciprocal relationship. ⋯ Mechanisms shown to regulate neuroplasticity and behavior in diabetes models, including stress hormones, neurotransmitters, neurotrophins, inflammation and aging, are integrated within this framework. Pathological changes in hippocampal function can contribute to the brain symptoms of diabetes-associated complications by failing to regulate the hypothalamic-pituitary-axis, maintain learning and memory and govern emotional expression. Further characterization of alterations in neuroplasticity along with glycemic control will facilitate the development and evaluation of pharmacological interventions that could successfully prevent and/or reverse the detrimental effects of diabetes on brain and behavior.