Neuroscience
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Physical exercise could exert a neuroprotective effect in both clinical studies and animal experiments. A series of related studies have indicated that physical exercise could reduce infarct volume, alleviate neurological deficits, decrease blood-brain barrier dysfunction, promote angiogenesis in cerebral vascular system and increase the survival rate after ischemic stroke. ⋯ Furthermore, it was demonstrated that exercise training could decrease the blood-brain barrier dysfunction and promote angiogenesis in cerebral vascular system. An awareness of the exercise intervention benefits pre- and post stroke may lead more stroke patients and people with high-risk factors to accept exercise therapy for the prevention and treatment of stroke.
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Head direction (HD) cells have been identified in a number of limbic system structures. These cells encode the animal's perceived directional heading in the horizontal plane and are dependent on an intact vestibular system. ⋯ These mechanisms are: (1) the ascending vestibular signal is generated by more than just vestibular-only neurons, (2) not all vestibular-only neurons contributing to the HD pathway have firing rates that are attenuated by active head turns, (3) the ascending pathway may be spared from the affects of the attenuation in that the HD system receives information from other vestibular brainstem sites that do not include vestibular-only cells, and (4) the ascending signal is affected by the inhibited vestibular signal during an active head turn, but the HD circuit compensates and uses the altered signal to accurately update the current HD. Future studies will be needed to decipher which of these possibilities is correct.
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Deficient reelin signaling leads to characteristic layering malformations in the cerebral cortex and causes polarity defects of cortical neurons. Since the discovery of reelin much has been learned about the molecular mechanisms that underlie the characteristic defects of layering defects in the reeler mutant. More recent studies provided insights in the crosstalk between reelin signaling and molecular pathways that control polarity development of radially migrating neurons. The present review summarizes and discusses recent findings on the role of reelin in modulating polarization and process orientation of neurons in the neocortex and hippocampus.
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The molecular and cellular mechanisms, which coordinate the critical stages of brain development to reach a normal structural organization with appropriate networks, are progressively being elucidated. Experimental and clinical studies provide evidence of the occurrence of developmental alterations induced by genetic or environmental factors leading to the formation of aberrant networks associated with learning disabilities. Moreover, evidence is accumulating that suggests that also late-onset neurological disorders, even Alzheimer's disease, might be considered disorders of aberrant neural development with pathological changes that are set up at early stages of development before the appearance of the symptoms. ⋯ In the present review we focus on (1) aspects of neurogenesis with relevance to aging; (2) neurodegenerative disease (NDD)-associated proteins/pathways in the developing brain; and (3) further pathways of the developing or neurodegenerating brains that show commonalities. Elucidation of complex pathogenetic routes characterizing the earliest stage of the detrimental processes that result in pathological aging represents an essential first step toward a therapeutic intervention which is able to reverse these pathological processes and prevent the onset of the disease. Based on the shared features between pathways, we conclude that prevention of NDDs of the elderly might begin during the fetal and childhood life by providing the mothers and their children a healthy environment for the fetal and childhood development.
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Oligodendrocyte precursor cells (OPC) are glial cells that metamorphose into myelinating oligodendrocytes during embryogenesis and early stages of post-natal life. OPCs continue to divide throughout adulthood and some eventually differentiate into oligodendrocytes in response to demyelinating lesions. ⋯ In this review, we summarize the interwoven factors and cascades that promote the activation, recruitment and differentiation of OPCs into myelinating oligodendrocytes in the adult brain based mostly on results found in the study of demyelinating diseases. The goal of the review was to draw a complete picture of the transformation of OPCs into mature oligodendrocytes to facilitate the study of this transformation in both the normal and diseased adult brain.