Neurobiology of DiseaseElsevier, 6. sep. 2011 - 1104 sider Neurobiology of Disease is aimed at any basic scientist or clinician scientist teaching a course or conducting research on the basic science underlying the major neurological diseases. It provides an excellent overview of cutting-edge research on the fundamental disorders of the nervous system, including physiological and molecular aspects of dysfunction. The major categories of neurological disease are covered, and the chapters provide specific information about particular diseases exemplifying each of these categories. Sufficient clinical information is included to put into perspective the basic mechanisms discussed. The book assembles a world-class team of section editors and chapters written by acknowledged experts in their respective fields.
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Side x
... Cognition and Behavior, Kennedy Krieger Institute Baltimore, Maryland Guido Cavaletti, MD Department of Neurosciences ... Cognitive Neurology, Kennedy Krieger Institute Baltimore, Maryland Rima M. Dafer, MD, MPH Department of Neurology ...
... Cognition and Behavior, Kennedy Krieger Institute Baltimore, Maryland Guido Cavaletti, MD Department of Neurosciences ... Cognitive Neurology, Kennedy Krieger Institute Baltimore, Maryland Rima M. Dafer, MD, MPH Department of Neurology ...
Side 46
... Cognitive decline occurs only late in the disease [56,58]. Computed tomographic (CT) and MRI findings are characterized by diffuse white-matter lesions that are predominant in the frontal lobe white matter associated with enlargement of ...
... Cognitive decline occurs only late in the disease [56,58]. Computed tomographic (CT) and MRI findings are characterized by diffuse white-matter lesions that are predominant in the frontal lobe white matter associated with enlargement of ...
Side 61
... cognitive decline. These systems exert their function via metabotropic receptors. A. Cholinergic. System. The cholinergic neurons, predominantly localized in the substantia innominata, are divided into eight neuronal groups, Ch1–Ch8, and ...
... cognitive decline. These systems exert their function via metabotropic receptors. A. Cholinergic. System. The cholinergic neurons, predominantly localized in the substantia innominata, are divided into eight neuronal groups, Ch1–Ch8, and ...
Side 75
... cognitive impairment remain unanswered. A is the principal constituent of both meningeal and capillary (parenchymal) CAA, as well as of SPs, the latter both containing mainly A-42 and showing statistically high correlation with neuritic ...
... cognitive impairment remain unanswered. A is the principal constituent of both meningeal and capillary (parenchymal) CAA, as well as of SPs, the latter both containing mainly A-42 and showing statistically high correlation with neuritic ...
Side 76
... cognitive functions is further accelerated as a result of interactions with APP processing. Extracellular A aggregation is suggested to affect cholinergic terminations before progression onto other neurotransmitter systems ...
... cognitive functions is further accelerated as a result of interactions with APP processing. Extracellular A aggregation is suggested to affect cholinergic terminations before progression onto other neurotransmitter systems ...
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abnormalities acid activity amyotrophic lateral sclerosis animal models antibodies antigens associated ataxia atrophy autism autoimmune axonal brain calcium cancer cause cellular central nervous system cerebellar cerebral chromosome Clin clinical cognitive cortex cortical creatine deficiency dementia dendritic diagnosis disorders dysfunction effects enzyme expression factors function gene genetic gliomas granule cell hippocampal human identified immune impairment increased infarction infection inflammatory involved lesions loss lymphoma lysosomal mechanisms medulloblastoma membrane meningiomas metabolism metastasis mice migraine mitochondrial molecular motor neuron mouse model multiple muscle mutations myelin myoclonus nerve neurological neuropathy Neurosci normal nucleus occur onset Parkinson’s disease pathogenesis pathology Pathophysiology pathways patients PCNSL phenotype potential primary prion progressive protein Purkinje cells receptor region response result role SCA1 seizures sodium channel spinal stroke studies subunit suggest symptoms syndrome synuclein systemic lupus erythematosus temporal lobe epilepsy therapy tion tissue transgenic treatment tumor vascular virus white matter
Populære passager
Side 410 - Alizadeh, AA, Eisen, MB, Davis, RE, Ma, C., Lossos, I. S., Rosenwald, A., Boldrick, JC, Sabet, H., Tran, T., Yu, X., Powell, JI, Yang, L., Marti, GE, Moore, T., Hudson, J.
Side 583 - ... marked impairment in the use of multiple nonverbal behaviors such as eye-to-eye gaze, facial expression, body postures, and gestures to regulate social interaction b. failure to develop peer relationships appropriate to developmental level c. a lack of spontaneous seeking to share enjoyment, interests, or achievements with other people (eg, by a lack of showing, bringing, or pointing out objects of interest) d.
Side 583 - A. Qualitative impairment in social interaction, as manifested by at least two of the following: (1) marked impairment in the use of multiple nonverbal behaviors such as eye-to-eye gaze, facial expression, body postures, and gestures to regulate social interaction (2) failure to develop peer relationships appropriate to developmental level (3) a lack of spontaneous seeking to share enjoyment...
Side 583 - ... play appropriate to developmental level (3) restricted repetitive and stereotyped patterns of behavior, interests, and activities, as manifested by at least one of the following: (a) encompassing preoccupation with one or more stereotyped and restricted patterns of interest that is abnormal either in intensity or focus (b) apparently inflexible adherence to specific, nonfunctional routines or rituals (c) stereotyped and repetitive motor mannerisms (eg, hand or finger flapping or twisting, or...
Side 532 - Gurney, ME, Pu, H., Chiu, AY, Dal Canto, MC, Polchow, CY, Alexander, DD, Caliendo, J., Hentati, A., Kwon, YW, Deng, HX, Chen, W., Zhai, P., Sufit, RL, and Siddique, T.
Side 533 - K. (1997). Epilepsy and exacerbation of brain injury in mice lacking the glutamate transporter GLT-1. Science 276, 1699-1702.
Side 240 - Atrial Fibrillation Investigators. Risk factors for stroke and efficacy of antithrombotic therapy in atrial fibrillation: analysis of pooled data from five randomized controlled trials.
Side 121 - Kruger R, Kuhn W, Muller T, Woitalla D, Graeber M, Kosel S, Przuntek H, Epplen JT, Schols L, Riess O.
Side 431 - Pomeroy SL, Tamayo P, Gaasenbeek M. Sturla LM, Angelo M, McLaughlin ME, Kim JY. Goumnerova LC, Black PM, Lau C. Allen JC. Zagzag D, Olson JM, Curran T, Wetmore C, Biegel JA. Poggio T. Mukherjee S. Rifkin R. Califano A, Stolovitzky G. Louis DN, Mesirov JP, Lander ES.
Side 533 - Oosthuyse, B., Moons, L., Storkebaum, E., Beck, H., Nuyens, D., Brusselmans, K., Van Dorpe, J., Hellings, P., Gorselink, M., Heymans, S., Theilmeier, G., Dewerchin, M., Laudenbach, V., Vermylen...