Impaired neurovascular coupling and cognitive deficits in anti-N-methyl-D-aspartate receptor encephalitis

2021 ◽  
Author(s):  
Yuanyuan Guo ◽  
Xinyi Lv ◽  
Qiang Wei ◽  
Yue Wu ◽  
Yue Chen ◽  
...  
Keyword(s):  
Cognitive Deficits ◽  
Neurovascular Coupling ◽  
Aspartate Receptor

scholarly journals Region-Specific Neurovascular Decoupling Associated With Cognitive Decline in Parkinson’s Disease

2021 ◽  
Vol 13 ◽  
Author(s):  
Song’an Shang ◽  
Hongying Zhang ◽  
Yuan Feng ◽  
Jingtao Wu ◽  
Weiqiang Dou ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cognitive Impairment ◽  
Cognitive Decline ◽  
Cognitive Deficits ◽  
Inferior Frontal Gyrus ◽  
Neurovascular Coupling ◽  
Angular Gyrus ◽  
Visual Spatial ◽  
The Right

Background: Cognitive deficits are prominent non-motor symptoms in Parkinson’s disease (PD) and have been shown to involve the neurovascular unit (NVU). However, there is a lack of sufficient neuroimaging research on the associated modulating mechanisms. The objective of this study was to identify the contribution of neurovascular decoupling to the pathogenesis of cognitive decline in PD.Methods: Regional homogeneity (ReHo), a measure of neuronal activity, and cerebral blood flow (CBF), a measure of vascular responses, were obtained from patients with PD with mild cognitive impairment (MCI) and normal cognition (NC) as well as matched healthy controls (HCs). Imaging metrics of neurovascular coupling (global and regional CBF-ReHo correlation coefficients and CBF-ReHo ratios) were compared among the groups.Results: Neurovascular coupling was impaired in patients with PD-MCI with a decreased global CBF-ReHo correlation coefficient relative to HC subjects (P < 0.05). Regional dysregulation was specific to the PD-MCI group and localized to the right middle frontal gyrus, right middle cingulate cortex, right middle occipital gyrus, right inferior parietal gyrus, right supramarginal gyrus, and right angular gyrus (P < 0.05). Compared with HC subjects, patients with PD-MCI showed higher CBF-ReHo ratios in the bilateral lingual gyri (LG), bilateral putamen, and left postcentral gyrus and lower CBF-ReHo ratios in the right superior temporal gyrus, bilateral middle temporal gyri, bilateral parahippocampal gyri, and right inferior frontal gyrus. Relative to the HC and PD-NC groups, the PD-MCI group showed an increased CBF-ReHo ratio in the left LG, which was correlated with poor visual–spatial performance (r = −0.36 and P = 0.014).Conclusion: The involvement of neurovascular decoupling in cognitive impairment in PD is regionally specific and most prominent in the visual–spatial cortices, which could potentially provide a complementary understanding of the pathophysiological mechanisms underlying cognitive deficits in PD.

scholarly journals Selected single-nucleotide variants in GRIN1, GRIN2A, and GRIN2B encoding subunits of the NMDA receptor are not biomarkers of schizophrenia resistant to clozapine: exploratory study

2020 ◽  
Author(s):  
Marek Krzystanek ◽  
Marek Asman ◽  
Joanna Witecka ◽  
Artur Pałasz ◽  
Ryszard Wiaderkiewicz
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Deficits ◽  
Exploratory Study ◽  
Study Group ◽  
Treatment Resistant ◽  
Single Nucleotide Variants ◽  
Chain Reaction ◽  
Single Nucleotide ◽  
Aspartate Receptor ◽  
Polymerase Chain

Abstract Background Schizophrenia is a common mental illness whose pathogenesis is still unknown. The vulnerability and stress model in schizophrenia assume that susceptibility to the disease is mainly associated with genes. Of the five symptomatic dimensions of schizophrenia, cognitive impairment appears to be most associated with the pathogenesis of schizophrenia. The aim of the study was to explore whether selected nucleotide variants in GRIN1, GRIN2A, and GRIN2B encoding subunits of the N-methyl-d-aspartate receptor (NMDA-R) receptor occur in a selected group of patients with treatment resistant schizophrenia with cognitive impairment. Methods The study included 45 patients diagnosed with super refractory schizophrenia, all with cognitive deficits and chronically psychotic. DNA fragments including the studied polymorphisms of the NMDA receptors subunit genes were amplified by polymerase chain reaction and subjected to sequencing. Results The study did not confirm the presence of any of the four selected single-nucleotide variants in GRIN1, GRIN2A, and GRIN2B subunits of NMDA-R in the study group. Conclusion Results of the study indicated that the selected single-nucleotide variants are not associated both with resistance to clozapine and the presence of cognitive deficits in schizophrenia. It is possible, however, that a more extensive sequencing along with analyzing the expression of these genes may reveal different single-nucleotide variants than those assumed in the study.

Hippocampal Dysfunction in Schizophrenia and Aberrant Hippocampal Synaptic Plasticity in Rodent Model Psychosis: a Selective Review

2019 ◽  
Author(s):  
Julia C. Bartsch ◽  
Björn H. Schott ◽  
Joachim Behr
Keyword(s):  
Synaptic Plasticity ◽  
Cognitive Deficits ◽  
Positive Symptoms ◽  
Clinical Perspective ◽  
Hippocampal Synaptic Plasticity ◽  
Aspartate Receptor ◽  
Hippocampal Dysfunction ◽  
Model Psychosis ◽  
Global Population ◽  
Review Current

AbstractSchizophrenia is a complex, heterogeneous psychiatric disorder that affects about 1% of the global population. Hippocampal dysfunction has been linked to both cognitive deficits and positive symptoms in schizophrenia. Here, we briefly review current findings on disrupted hippocampal processing from a clinical perspective before concentrating on preclinical studies of aberrant hippocampal synaptic plasticity using the N-methyl-D-aspartate receptor hypofunction model of psychosis and related findings from genetic models. Taken together, the results put the case for maladaptive hippocampal synaptic plasticity and its extrinsic connections as mechanistic underpinnings of cognitive impairments in schizophrenia.

scholarly journals Exploratory study of selected nucleotide variants in GRIN1, GRIN2A and GRIN2B encoding subunits of the NMDA receptor in a targeted group of schizophrenia patients with chronic cognitive impairment

2020 ◽  
Author(s):  
Marek Krzystanek ◽  
Marek Asman ◽  
Joanna Witecka ◽  
Artur Pałasz ◽  
Ryszard Wiaderkiewicz
Keyword(s):  
Nmda Receptor ◽  
Cognitive Deficits ◽  
Mental Disease ◽  
Psychotic Episode ◽  
Single Nucleotide Variants ◽  
Single Nucleotide ◽  
First Psychotic Episode ◽  
Aspartate Receptor ◽  
Polymerase Chain ◽  
Symptomatic Remission

Abstract Background Schizophrenia is a mental disease that affects approximately 1% of the population. Despite over 100 years of research, its pathomechanism has still not been clarified. Cognitive deficits, which are one of the symptomatic dimensions of schizophrenia, usually appear a few years before the first psychotic episode. Therefore, this is why they are probably the clinical manifestation of the primary pathomechanism of schizophrenia. It is also supposed that N-methyl-d-aspartate receptor (NMDA-R) insufficiency in the prefrontal cortex is responsible for cognitive deficits in schizophrenia. The study aimed to examine whether four selected single nucleotide variants in GRIN1, GRIN2A and GRIN2B encoding NMDA-R subunits, of which two have not been tested before, are linked with the selected clinical phenotype of cognitive dysfunction in schizophrenia. Methods The study included the targeted group of 117 patients diagnosed with schizophrenia, all with cognitive deficits and in symptomatic remission. DNA fragments including the studied polymorphisms of the NMDA receptors subunit genes were amplified by polymerase chain reaction and subjected to sequencing. Results The study did not confirm the presence of any of the four selected single nucleotide variants in GRIN1, GRIN2A and GRIN2B subunits of NMDA-R. Conclusions The finding indicates that selected single nucleotide variants in GRIN2A and GRIN2B encoding subunits of the NMDA receptor are not associated with the presence of cognitive deficits in schizophrenia.

Permanent deficits in brain functions caused by long-term ketamine treatment in mice

2010 ◽  
Vol 30 (9) ◽  
pp. 1287-1296 ◽  
Author(s):  
L Sun ◽  
WP Lam ◽  
YW Wong ◽  
LH Lam ◽  
HC Tang ◽  
...  
Keyword(s):  
Working Memory ◽  
Prefrontal Cortex ◽  
Cognitive Deficits ◽  
Long Term Effects ◽  
Post Dose ◽  
Significant Deterioration ◽  
Competitive Antagonist ◽  
Brain Functions ◽  
Aspartate Receptor

Ketamine, an injectable anesthetic, is also a popular recreational drug used by young adults worldwide. Ketamine is a non-competitive antagonist of N-methyl-d-aspartate receptor, which plays important roles in synaptic plasticity and neuronal learning. Most previous studies have examined the immediate and short-term effects of ketamine, which include learning and cognitive deficits plus impairment of working memory, whereas little is known about the long-term effects of repeated ketamine injections of common or usual recreational doses. Therefore, we aimed to evaluate the deficits in brain functions with behavioral tests, including wire hang, hot plate and water maze tests, plus examine prefrontal cortex apoptotic markers, including Bax, Bcl-2 and caspase-3, in mice treated with 6 months of daily ketamine administration. In our study, following 6 months of ketamine injection, mice showed significant deterioration in neuromuscular strength and nociception 4 hours post-dose, but learning and working memory were not affected nor was there significant apoptosis in the prefrontal cortex. Our research revealed the important clinical finding that long-term ketamine abuse with usual recreational doses can detrimentally affect neuromuscular strength and nociception as part of measurable, stable and persistent deficits in brain function.

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