Neuronal dysfunction

It is unclear whether the myopathy was a direct toxic effect of chlordecone on the muscle or whether the myopathy was a consequence of neuronal dysfunction. In addition, arthralgia in the proximal joints was reported by 4 of 23 workers with active symptoms of chlordecone intoxication (Taylor 1982, 1985). No cause for the joint pain could be determined. 

Neuronal dysfunction associated with nutritional deficiency... 

Lewy bodies (LB) are neuronal inclusions, composed of abnormal neurofilament and synaptic proteins, thought to be surrogate markers for neuronal dysfunction and eventual cell death. They are found in diverse locations including cholinergic and monoaminergic neurons of the brainstem, diencephalon. 

Hallett, J.J., Harling-Berg, C.J., Knopf, P.M., Stopa, E.G., and Kiessling, L.S. (2000) Anti-striatal antibodies in Tourette syndrome cause neuronal dysfunction. / Neuroimmunol 111 195—202. 

The PA4 peptide and an excessive amount of APP have proved to be neurotoxic. The accumulation of the pA4 peptide between synapses may be responsible for neuronal dysfunction and death (Schubert et al. 1991). PA4 could also modify the N-methyl-D-aspartate (NMDA) receptor, making possible the presence of neurotoxicity via the excitotoxin and calcium pathways [Mattson et al. 1992). Drugs that interfere with these pathways or alter calcium homeostasis have a potential therapeutic role. 

S100B Overexpression Female specific hyperactivity, lack of habituation to novelty, reduced T-maze spontaneous alternation rate, abnormal exploratory behavior Enhanced astrocytosis and neurite proliferation Impaired learning and memory, increased dendrite density, enhanced age-related loss of dendrites Inhibitory effect on cardiac hypertrophy Increased susceptibility to hypoxia-ischemia Increased apoptosis after myocardial infarction Enhanced neuroinflammation and neuronal dysfunction induced by amyloid-(3... 

Stavrovskaya, I.G. and Kristal, B. S., 2005, The powerhouse takes control of the cell is the mitochondrial permeability transition a viable therapeutic target against neuronal dysfunction and death , Free Rad. Biol. Med. 38, pp. 687-697... 

Nabeshima, T., and Nitta, A. (1994). Memory impairment and neuronal dysfunction induced by beta-amyloid protein in rats. Tohoku J Exp Med 174, 241—249. 

Neuronal dysfunction on FDG-PET/fMRI -High CSF tau/p-tau -Cortical thinning/Hippocampal atrophy on sMRI. 

Deicken RF, Zhou L, Schuff N, Fein G, Weiner MW. 1998. Hippocampal neuronal dysfunction in schizophrenia as measured by proton magnetic resonance spectroscopy. Biol Psychiatry 43 483-488. 

Ohrmann P, Siegmund A, Suslow T, Spitzberg K, Kersting A, et al. 2005. Evidence for glutamatergic neuronal dysfunction in the prefrontal cortex in chronic but not in first-episode patients with schizophrenia A proton magnetic resonance spectroscopy study. Schizophr Res 73 153-157. 

Evidence for neuronal dysfunction in the anterior cingulate of patients with schizophrenia A proton magnetic resonance spectroscopy study at 31. Schizophr Res 94 328-331. 

The value of the correlation coefficient for the data shown in Fig. 13.9 shows that the probability that neuronal dysfunction is not related directly to the aggregation of the Ap-peptide, in this system at least, is less than 1 in... 

The availability of genetically modified mice has advanced our understanding of several neurodegenerative processes. Cellular neurobiology experiments have informed us about mechanisms of neuronal dysfunction in AD and PD mouse models. For instance, recent studies have identified that synaptic transmission is one of the earliest events in the cognitive abnormalities that characterize AD and PD. The integration of this information with data-based circuits modeling, in which neuronal electrical properties, synaptic transmission parameters, and brain oscillations can now be evaluated and it has been recently addressed in PD and AD. 

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