Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alzheimer's disease is characterized by markedly reduced concentration of acetylcholine in hippocampus and neocortex, caused by degeneration of cholinergic neurons. Acetylcholine is essential in learning and memory. However, despite correlation between cholinergic defect and intellectual impairment in Alzheimer's disease, the effect of substitution therapy with cholinergics is very limited. Especially in younger Alzheimer patients, the degenerative process also affects other transmitter systems. Particularly the concentrations of serotonin, somatostatin and glutamate are significantly reduced. It is not elucidated how these transmitter defects contribute to symptomatology. The serotonin defect is thought to underlie the emotional and behavioural symptoms. The somatostatin defect is correlated to the reduced cerebral metabolism and thus might be a central phenomenon. The glutamate defect has been suggested to represent the neurochemical correlate to clinical dementia, because the activity in the hippocampal glutamatergic synapses is normally increased during learning. Therapeutically, the multiple transmitter defects imply that simple transmitter substitution can be expected to be of only limited value in Alzheimer's disease.
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PMID:[Neurotransmitters in Alzheimer's disease]. 197 61

Senile dementia of the Alzheimer type is a chronic, progressive neuropsychiatric condition characterized clinically by global intellectual impairment and neuropathologically by the presence of numerous argyrophilic plaques and tangles. Neurochemical investigations have established loss of the cholinergic and aminergic projections to the cerebral cortex and a loss of the content of somatostatin, with preservation of cholecystokinin and vasoactive intestinal polypeptide, neuropeptides also located in cells intrinsic to the cortex. We describe here the relationship between cortical somatostatin immunoreactivity and the plaques and tangles of diseased tissue by immunocytochemical and silver impregnation techniques on paraffin-embedded tissue. In sections of Alzheimer's tissue, cortical somatostatin-immunoreactive perikarya exhibited morphological changes consistent with neuronal degeneration. Silver-stained material immunostained subsequently showed that many neurones containing tangles were also somatostatin positive. No such colocalization was observed using antisera to other neuropeptides. Our findings indicate that a subclass of somatostatin-positive neurones are affected selectively in Alzheimer's disease and that these neurones also contain neuronal tangles. Thus, destruction of somatostatin-containing neurones is an early and perhaps critical event in the disease process.
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PMID:Location of neuronal tangles in somatostatin neurones in Alzheimer's disease. 285 57

Somatostatin-like immunoreactivity in Alzheimer CSF was significantly lower than in that from age-matched controls. The degree of reduction correlated with indices of intellectual impairment and decline in cortical glucose utilization as determined by PET. There was a close association between reduction in CSF somatostatin and glucose hypometabolism in the parietal lobe. In postmortem cortical tissue from Alzheimer patients, somatostatin levels were lower in posterior parietal but not in anterior frontal cortex. Loss of somatostatin-containing neurons, especially in the parietal association cortex, may be a critical determinant for Alzheimer dementia.
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PMID:Alzheimer's disease: low cerebral somatostatin levels correlate with impaired cognitive function and cortical metabolism. 287 58

Dementia of the Alzheimer type (DTA) is the most common form of adult-onset dementia. The clinical features of the disease include progressive memory defect, intellectual impairment and behavioral disturbances. The number of patients suffering from DTA is increasing dramatically, due to the growing proportion of old people. DTA therefore is a major public health problem. Brain lesions include several histopathological changes (mostly in the cerebral cortex and hippocampus): neurofibrillary tangles, senile plaques, granulo-vacuolar degeneration, Hirano bodies, angiopathy, loss of nerve cells. Postmortem brain examination reveals characteristic neurochemical deficits. The most consistent reduction in neurotransmitter-synthesizing enzyme observed so far is a reduction in choline acetyltransferase activity, suggesting a cholinergic deficit. However, other deficits involving noradrenaline and somatostatin have also been reported. Several hypotheses (genetic, viral, toxic, immunologic, metabolic) have been put forward in order to explain DTA. The relationship between these hypotheses and the neurochemical deficits is still unclear, but the existence of characteristic neurotransmitter-related deficits allows specific therapeutic trials.
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PMID:[Alzheimer's type dementia: recent data]. 613 79