Reciprocal changes in corticotropin-releasing factor (CRF)-like immunoreactivity and CRF receptors in cerebral cortex of Alzheimer's disease

Alzheimer's disease is a progressive degenerative disease of the nervous system characterized neuropathologically by the presence of senile plaques and neurofibrillary tangles in amygdala, hippocampus and neocortex. Dysfunction and death of basal forebrain cholinergic neurones projecting to forebrain targets are associated with marked decreases in cholinergic markers, including the activity of choline acetyltransferase (ChAT). Although cortical levels of somatostatin and somatostatin receptors are reduced in Alzheimer's, no consistent changes have been reported in other neuropeptide systems. We have now examined in control and Alzheimer's brain tissues pre- and postsynaptic markers of corticotropin-releasing factor (CRF), a hypothalamic peptide regulating pituitary-adrenocortical secretion which also seems to act as a neurotransmitter in the central nervous system (CNS). We have found that in Alzheimer's, the concentrations of CRF-like immunoreactivity (CRF-IR) are reduced and that there are reciprocal increases in CRF receptor binding in affected cortical areas. These changes are significantly correlated with decrements in ChAT activity. Our results strongly support a neurotransmitter role for CRF in brain and demonstrate, for the first time, a modulation of CNS CRF receptors associated with altered CRF content. These observations further suggest a possible role for CRF in the pathophysiology of the dementia. Future therapies directed at increasing CRF levels in brain may prove useful for treatment.     

Three-dimensional recon- struction and analysis of structure characteristics on senile plaques of Alzheimer’s disease

Alzheimer‘s disease is a progressive neurodegenerative disorder characterized by the presence of senile plaques primarily composed of amyloid β in brain. Abnor-mal secretion and aggregation of amyloid β are the key events in pathogenesis of Alzheimer‘s disease. Reduction of amyloid β production and inhibition of amyloid β aggregation to form senile plaques are hopeful strategies for the treatment and prevention of Alzheimer‘s disease. In the present study, the silver and immunohistochemical staining methods were applied to discover senile plaques in the hippocampus of Alzheimer‘s disease patients, and then images were processed and three-dimensionally reconstructed by Matlab and AVS software. The structure characteristics of senile plaques were measured through correlation function calculation and fractal dimension by a computer-aided method. Diffuse plaque had no amyloid center, but classic plaque presented compact central core structure; two types of plaques were both of porous structure, but the sizes of their pores were significantly different. Furthermore, there was difference in fractal dimension value between the diffuse plaque and classic plaque in the two staining methods. The comparison of structure characteristics between two types of plaques indicated that they developed independently. Establishment of the methods for reconstructing the three-dimensional structure of senile plaque and analyzing their structure characteristics is helpful for further study on the aggregation mechanism of senile plaque.     

老年甲状腺功能亢进性心脏病34例临床分析

目的探讨老年甲状腺功能亢进性心脏病的临床诊疗特点.方法回顾性分析34例老年甲亢性心脏病患者的临床表现、误诊情况及治疗.结果30例显性甲亢并甲心病患者,症状明显好转或消失27例(90.0%),18例房颤、房扑中11例在治疗过程中恢复为窦性心率(61.1%).结论60岁以上的患者出现不明原因的心律失常,常规治疗效果欠佳,应考虑到甲状腺功能亢进性心脏病的可能,甲亢完全控制后心脏功能可明显好转或恢复正常.     

老年甲状腺功能亢进性心脏病34例临床分析

目的探讨老年甲状腺功能亢进性心脏病的临床诊疗特点.方法回顾性分析34例老年甲亢性心脏病患者的临床表现、误诊情况及治疗.结果30例显性甲亢并甲心病患者,症状明显好转或消失27例(90.0%),18例房颤、房扑中11例在治疗过程中恢复为窦性心率(61.1%).结论60岁以上的患者出现不明原因的心律失常,常规治疗效果欠佳,应考虑到甲状腺功能亢进性心脏病的可能,甲亢完全控制后心脏功能可明显好转或恢复正常.     

Analgesia and hyperalgesia from GABA-mediated modulation of the cerebral cortex

It is known that pain perception can be altered by mood, attention and cognition, or by direct stimulation of the cerebral cortex, but we know little of the neural mechanisms underlying the cortical modulation of pain. One of the few cortical areas consistently activated by painful stimuli is the rostral agranular insular cortex (RAIC) where, as in other parts of the cortex, the neurotransmitter gamma-aminobutyric acid (GABA) robustly inhibits neuronal activity. Here we show that changes in GABA neurotransmission in the RAIC can raise or lower the pain threshold--producing analgesia or hyperalgesia, respectively--in freely moving rats. Locally increasing GABA, by using an enzyme inhibitor or gene transfer mediated by a viral vector, produces lasting analgesia by enhancing the descending inhibition of spinal nociceptive neurons. Selectively activating GABA(B)-receptor-bearing RAIC neurons produces hyperalgesia through projections to the amygdala, an area involved in pain and fear. Whereas most studies focus on the role of the cerebral cortex as the end point of nociceptive processing, we suggest that cerebral cortex activity can change the set-point of pain threshold in a top-down manner.     

中枢型尼古丁受体与阿尔茨海默病

阿尔茨海默病是一种以渐进性的认知功能障碍为主要特征的神经退行性疾病，该病最终会导致死亡，是痴呆病中最常见的一种类型。近年来研究发现中枢尼古丁受体在AD的发病中起着非常重要的作用，本文对此进行综述。     

The colour centre in the cerebral cortex of man

Anatomical and physiological studies have shown that there is an area specialized for the processing of colour (area V4) in the prestriate cortex of macaque monkey brain. Earlier this century, suggestive clinical evidence for a colour centre in the brain of man was dismissed because of the association of other visual defects with the defects in colour vision. However, since the demonstration of functional specialization in the macaque cortex, the question of a colour centre in man has been reinvestigated, based on patients with similar lesions in the visual cortex. In order to study the colour centre in normal human subjects, we used the technique of positron emission tomography (PET), which measures increases in blood flow resulting from increased activity in the cerebral cortex. A comparison of the results of PET scans of subjects viewing multi-coloured and black-and-white displays has identified a region of normal human cerebral cortex specialized for colour vision.     

Single-cell atlas of domestic pig cerebral cortex and hypothalamus

The brain of the domestic pig(Sus scrofa domesticus)has drawn considerable attention due to its high similarities to that of humans.However,the cellular composi...     

Calbindin immunoreactivity alternates with cytochrome c-oxidase-rich zones in some layers of the primate visual cortex

Calcium ions have a pivotal role in many neuronal activities, but little is known about their involvement in the cortical processing of visual information. Using immunohistochemical methods, we have now detected a calcium-binding protein, calbindin-D-28K, which may confer on certain compartments of cortical area 17 the ability to modulate Ca2+ metabolism. Thus, calbindin occurs in the primate striate cortex in a pattern almost complementary to that displaying strong cytochrome c-oxidase activity. From this and other observations, we deduce that the distribution of calbindin-immunoreactive sites corresponds mainly to extra-geniculocortical connections of the primary visual cortex. This implies that the geniculocortical and extra-geniculocortical compartments of area 17 differ in an intracellular system for Ca2+ homeostasis.