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Query: UMLS:C0025362 (mental retardation)
 15,878 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Most people are aware of subtle differences in cognitive functions between men and women. Psychometric tests confirm specific gender differences in a number of areas, the most robust being in spatial orientation and mathematical tasks which are better performed by males. Nonetheless, normal males and females perform comparably on intelligence tests and human brains lack sexual dimorphism on routine neuropathological exams--other than mean differences in weight and size. Even so, human brains demonstrate: 1) a sexually dimorphic nucleus in the hypothalamus with twofold neuronal numbers in males than in females; 2) the planum temporale/anterior Sylvian fissure on the left side are larger in males; 3) some studies reveal the posterior corpus callosum to be more bulbous in females while others fail to show this difference; and 4) a cytoarchitectural study demonstrates definite sexual dimorphism of cerebral cortex with significantly higher neuronal densities and neuronal number estimates in males and a reciprocal increase in neuropil/neuronal processes in female cortex as implied by the 2 sexes' similar mean cortical thicknesses. Such morphologic differences may provide the structural underpinning for the gender differences exhibited by the normal and diseased brain. Males manifest a higher prevalence of mental retardation and of learning disabilities than females which may reflect the male fetus' smaller overproduction of nerve cells. Such an inference is supported by the demonstration of 1) better functional recovery following early brain injury than after later insults, 2) substantially overproduced and secondarily reduced nerve cells in human cerebral cortex during gestation, 3) the demonstration of a similar neuronal production and a testosterone-dependent neuronal involution of the sexually dimorphic hypothalamic nucleus in rats, and 4) more cortical neurons present in the adult human male than female. If an overproduced nerve cell population is capable of compensating for pathologic nerve cell losses taking place during the process of neuronal involution, the magnitude of overproduced nerve cells may define the extent of the protection conveyed. Because male fetuses appear to involute fewer overproduced cortical neurons than females, this gender difference could explain in part the boys' greater functional impairments from early brain damage. Women, on the other hand, exhibit a higher incidence and prevalence of dementia than do men. Given the females' overall larger extent of cortical neuropil (neuronal processes) and lower neuronal numbers compared with men, any disease that causes neuronal loss could be expected to lead to more severe functional deficits in women due to their loss of more dendritic connections per neuron lost. In conclusion, superimposed on a strong background of functional and structural equality, human male and female cerebral cortex display distinct, sexually dimorphic features, which can begin to be linked to a complex array of gender-specific advantages and limitations in cognitive functions.
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PMID:The human cerebral cortex: gender differences in structure and function. 1019 13

Hypoxic-ischemic encephalopathy (HIE) at birth could cause cerebral palsy (CP), mental retardation, and epilepsy, which last throughout the individual's lifetime. However, few restorative treatments for ischemic tissue are currently available. Cell replacement therapy offers the potential to rescue brain damage caused by HI and to restore motor function. In the present study, we evaluated the ability of embryonic stem cell-derived neural progenitor cells (ES-NPCs) to become cortical deep layer neurons, to restore the neural network, and to repair brain damage in an HIE mouse model. ES cells stably expressing the reporter gene GFP are induced to a neural precursor state by stromal cell co-culture. Forty-hours after the induction of HIE, animals were grafted with ES-NPCs targeting the deep layer of the motor cortex in the ischemic brain. Motor function was evaluated 3 weeks after transplantation. Immunohistochemistry and neuroanatomical tracing with GFP were used to analyze neuronal differentiation and axonal sprouting. ES-NPCs could differentiate to cortical neurons with pyramidal morphology and expressed the deep layer-specific marker, Ctip2. The graft showed good survival and an appropriate innervation pattern via axonal sprouting from engrafted cells in the ischemic brain. The motor functions of the transplanted HIE mice also improved significantly compared to the sham-transplanted group. These findings suggest that cortical region specific engraftment of preconditioned cortical precursor cells could support motor functional recovery in the HIE model. It is not clear whether this is a direct effect of the engrafted cells or due to neurotrophic factors produced by these cells. These results suggest that cortical region-specific NPC engraftment is a promising therapeutic approach for brain repair.
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PMID:Cortical region-specific engraftment of embryonic stem cell-derived neural progenitor cells restores axonal sprouting to a subcortical target and achieves motor functional recovery in a mouse model of neonatal hypoxic-ischemic brain injury. 2397 Aug 53