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Fogelson N.,University of La Coruna | Fogelson N.,The Joseph Sagol Neuroscience Center
Neuroscience and Biobehavioral Reviews | Year: 2015

The objective of the current review is to integrate information from a series of studies, employing a paradigm that evaluates local contextual processing using electrophysiological measures. Collectively these studies provide an overview of how utilization of predictive context changes as a function of stimulus modality and across different patient populations, as well as the networks that may be critical for this function. The following aspects of local contextual processing will be discussed and reviewed: (i) the correlates associated with contextual processing that have been identified in healthy adults, (ii) stimulus modality effects, (iii) specific alterations and deficits of local contextual processing in aging and across different neurological and psychiatric patient populations, including patients with prefrontal cortex lesions, Parkinson's disease, schizophrenia, and major depressive disorder, (iv) the potential for utilizing the correlates of local context as biomarkers for frontal cognitive dysfunction and (v) the role of frontal networks in the processing of contextual information. Overall findings show that behavioral and neural correlates associated with processing of local context are comparable across stimulus modalities, but show specific alterations in aging and across different neurological and psychiatric disorders. © 2015 Elsevier Ltd. Source

Greenbaum L.,Sheba Medical Center at Tel Hashomer | Greenbaum L.,The Joseph Sagol Neuroscience Center | Lerer B.,Hebrew University of Jerusalem
Frontiers in Neurology | Year: 2015

Antipsychotic-induced movement disorders are major side effects of antipsychotic drugs among schizophrenia patients, and include antipsychotic-induced parkinsonism (AIP) and tardive dyskinesia (TD). Substantial pharmacogenetic work has been done in this field, and several susceptibility variants have been suggested. In this paper, the genetics of antipsychotic-induced movement disorders is considered in a broader context. We hypothesize that genetic variants that are risk factors for AIP and TD may provide insights into the pathophysiology of motor symptoms in Parkinson's disease (PD). Since loss of dopaminergic stimulation (albeit pharmacological in AIP and degenerative in PD) is shared by the two clinical entities, genes associated with susceptibility to AIP may be modifier genes that influence clinical expression of PD motor sub-phenotypes, such as age at onset, disease severity, or rate of progression. This is due to their possible functional influence on compensatory mechanisms for striatal dopamine loss. Better compensatory potential might be beneficial at the early and later stages of the PD course. AIP vulnerability variants could also be related to latent impairment in the nigrostriatal pathway, affecting its functionality, and leading to subclinical dopaminergic deficits in the striatum. Susceptibility of PD patients to early development of L-DOPA induced dyskinesia (LID) is an additional relevant sub-phenotype. LID might share a common genetic background with TD, with which it shares clinical features. Genetic risk variants may predispose to both phenotypes, exerting a pleiotropic effect. According to this hypothesis, elucidating the genetics of antipsychotic-induced movement disorders may advance our understanding of multiple aspects of PD and it clinical course, rendering this a potentially rewarding field of study. © 2015 Greenbaum and Lerer. Source

Boussi-Gross R.,The Institute of Hyperbaric Medicine | Golan H.,Nuclear Medicine Institute | Volkov O.,Nuclear Medicine Institute | Bechor Y.,The Institute of Hyperbaric Medicine | And 7 more authors.
Neuropsychology | Year: 2015

Objective: Several recent studies have shown that hyperbaric oxygen (HBO2) therapy carry cognitive and motor therapeutic effects for patients with acquired brain injuries. The goal of this study was to address the specific effects of HBO2 on memory impairments after stroke at late chronic stages. Method: A retrospective analysis was conducted on data of 91 stroke patients 18 years or older (mean age ~60 years) who had either ischemic or hemorrhagic stroke 3-180 months before HBO2 therapy (M = 30-35 months). The HBO2 protocol included 40 to 60 daily sessions, 5 days per week, 90 min each, 100% oxygen at 2ATA, and memory tests were administered before and after HBO2 therapy using NeuroTrax's computerized testing battery. Assessments were based on verbal or nonverbal, immediate or delayed memory measures. The cognitive tests were compared with changes in the brain metabolic state measured by single-photon emission computed tomography. Results: Results revealed statistically significant improvements (p < .0005, effect sizes medium to large) in all memory measures after HBO2 treatments. The clinical improvements were well correlated with improvement in brain metabolism, mainly in temporal areas. Conclusions: Although further research is needed, the results illustrate the potential of HBO2 for improving memory impairments in poststroke patients, even years after the acute event. © 2014 American Psychological Association. Source

Guerrero-Berroa E.,Mount Sinai School of Medicine | Schmeidler J.,Mount Sinai School of Medicine | Beeri M.S.,Mount Sinai School of Medicine | Beeri M.S.,The Joseph Sagol Neuroscience Center
European Neuropsychopharmacology | Year: 2014

Postmortem studies have shown that cerebrovascular disease (CVD) neuropathology occurs frequently in type 2 diabetes (T2D) through mechanisms associated with chronic hyperglycemia such as advanced glycation end-products (AGEs). The involvement of T2D in Alzheimer's disease (AD)-type neuropathology has been more controversial. While postmortem data from animal studies have supported the involvement of T2D in AD-type neuropathology through insulin mechanism that may affect the development of neuritic plaques and neurofibrillary tangles (NFTs), findings from postmortem studies in humans, of the association of T2D with AD, have been mainly negative. To complicate matters, medications to treat T2D have been implicated in reduced AD-type neuropathology. In this review we summarize the literature on animal and human postmortem studies of T2D neuropathology, mainly the mechanisms involved in hyperglycemia-related CVD neuropathology and hyperinsulinemia-related AD-type neuropathology. © 2014 Elsevier B.V. and ECNP. Source

Otahal J.,Academy of Sciences of the Czech Republic | Folbergrova J.,Academy of Sciences of the Czech Republic | Kovacs R.,Charite - Medical University of Berlin | Kunz W.S.,University of Bonn | And 2 more authors.
International Review of Neurobiology | Year: 2014

Epilepsy is one of the most common neurologic disorders affecting a substantial part of the population worldwide. Epileptic seizures represent the situation of increased neuronal activity associated with the enhanced demands for sufficient energy supply. For that purpose, very efficient regulatory mechanisms have to operate to ensure that cerebral blood flow, delivery of oxygen, and nutrients are continuously adapted to the local metabolic needs. The sophisticated regulation has to function in concert at several levels (systemic, tissue, cellular, and subcellular). Particularly, mitochondria play a key role not only in the energy production, but they are also central to many other processes including those leading to neuronal death. Impairment of any of the involved pathways can result in serious functional alterations, neurodegeneration, and potentially in epileptogenesis. The present review will address some of the important issues concerning vascular and metabolic changes in pathophysiology of epilepsy. © 2014 Elsevier Inc. Source

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