Atrophic Pattern of Hippocampal Subfields in Post-Stroke Demented Patient

2021 ◽  
pp. 1-11
Author(s):  
Zhiyong Zhao ◽  
Huaying Cai ◽  
Weihao Zheng ◽  
Tingting Liu ◽  
Di Sun ◽  
...  
Keyword(s):  
Sex Education ◽  
Cell Layer ◽  
Classification Performance ◽  
Asymmetry Index ◽  
Granule Cell Layer ◽  
Intracranial Volume ◽  
Hippocampal Subfields ◽  
Post Stroke ◽  
Positive Correlations ◽  
Atrophic Pattern

Background: Previous studies have demonstrated that hippocampal atrophy is a hallmark of dementia and can be used to predict the outcome of post-stroke demented (PSD) patients. The hippocampus consists of several subfields but their involvement in the pathophysiology of the PSD remains unclear. Objective: The present study aimed to investigate volumetric alterations of hippocampal subfields in patients with PSD. Methods: High-resolution T1-weighted images were collected from 27 PSD and 28 post-stroke nondemented (PSND) patients who recovered from ischemic stroke, and 17 age-matched normal control (NC). We estimated the volumes of the hippocampal subfields using FreeSurfer 6.0 which segmented the hippocampus into 12 subfields in each hemisphere. The volumetric differences between the groups were evaluated by the two-sample tests after regressing out the age, sex, education, and total intracranial volume. Results: Compared with NC group, PSD group showed smaller volumes in the entire hippocampus and its subfields, and such differences were not found in PSND group. Moreover, we found the dementia-specific atrophy in the left granule cell layer of dentate gyrus (GC-DG) and CA4 in the PSD patients compared with NC and PSND. Regression analysis showed positive correlations between the changes of cognitive performance and the asymmetry index in the CA3/4 and GC-DG of the PSD group. Furthermore, we found that the volumes of hippocampal subfields provided a better classification performance than the entire hippocampus. Conclusion: Our findings suggest that the hippocampus is reduced in the PSD patients and it presents a selective subfield involvement.

Cognitive Deficits and Clinical Symptoms with Hippocampal Subfields in First-Episode and Never-Treated Patients with Schizophrenia

2020 ◽  
Vol 31 (1) ◽  
pp. 89-96
Author(s):  
Mei Hong Xiu ◽  
XiaoE Lang ◽  
Da Chun Chen ◽  
Bo Cao ◽  
Thomas R Kosten ◽  
...  
Keyword(s):  
Regression Analysis ◽  
Cognitive Deficits ◽  
Clinical Symptoms ◽  
Molecular Layer ◽  
Verbal Learning ◽  
Multivariate Regression Analysis ◽  
Granule Cell Layer ◽  
First Episode ◽  
Intracranial Volume ◽  
Hippocampal Subfields

Abstract Memory dysfunction and associated hippocampal disturbances play crucial roles in cognitive impairment of schizophrenia. To examine the relationships between cognitive function and the hippocampal subfields (HSs) in first-episode never-treated (FENT) schizophrenia patients, the HSs were segmented in 39 FENT patients and 30 healthy controls using a state-of the-art automated algorithm. We found no significant differences in any HSs between the patients and controls. However, multivariate regression analysis showed that the left cornu ammonis 1 (CA1), left hippocampal tail, left presubiculum, and right molecular layer contributed 40% to the variance of the PANSS negative symptom score. After adjusting for sex, age, education, and intracranial volume, the partial correlation analysis showed that the volumes of left CA1, CA3, CA4, molecular layer, granule cell layer and both left and right subiculum were negatively correlated with the MATRICS consensus cognitive battery (MCCB) Hopkins Verbal Learning Test (HVLT). Multiple regression analysis showed that the left CA1 and CA3 hippocampal abnormalities contributed 66% to the variance of the HVLT. Our results suggest no detectable HS deficits were found in FENT schizophrenia patients. However, the HSs may be involved in the symptoms and cognitive deficits of schizophrenia patients in the early phase of their illness.

scholarly journals Cortical Volume, Thickness, and Surface Area in the Motoric Cognitive Risk Syndrome

2021 ◽  
pp. 1-14
Author(s):  
Helena M. Blumen ◽  
Emily Schwartz ◽  
Gilles Allali ◽  
Olivier Beauchet ◽  
Michele Callisaya ◽  
...  
Keyword(s):  
Surface Area ◽  
Sex Education ◽  
Cortical Thickness ◽  
Clinical Stage ◽  
White Matter Lesions ◽  
Cortical Atrophy ◽  
Intracranial Volume ◽  
Cortical Volume ◽  
Cognitive Risk ◽  
Cognitive Complaint

Background: The motoric cognitive risk (MCR) syndrome is a pre-clinical stage of dementia characterized by slow gait and cognitive complaint. Yet, the brain substrates of MCR are not well established. Objective: To examine cortical thickness, volume, and surface area associated with MCR in the MCR-Neuroimaging Consortium, which harmonizes image processing/analysis of multiple cohorts. Methods: Two-hundred MRIs (M age 72.62 years; 47.74%female; 33.17%MCR) from four different cohorts (50 each) were first processed with FreeSurfer 6.0, and then analyzed using multivariate and univariate general linear models with 1,000 bootstrapped samples (n-1; with resampling). All models adjusted for age, sex, education, white matter lesions, total intracranial volume, and study site. Results: Overall, cortical thickness was lower in individuals with MCR than in those without MCR. There was a trend in the same direction for cortical volume (p = 0.051). Regional cortical thickness was also lower among individuals with MCR than individuals without MCR in prefrontal, insular, temporal, and parietal regions. Conclusion: Cortical atrophy in MCR is pervasive, and include regions previously associated with human locomotion, but also social, cognitive, affective, and motor functions. Cortical atrophy in MCR is easier to detect in cortical thickness than volume and surface area because thickness is more affected by healthy and pathological aging.

scholarly journals Morphological Alterations in the Cerebellar Granule Cell Layer of Mice Lacking Calretinin

2011 ◽  
Vol 100 (3) ◽  
pp. 82a
Author(s):  
Don Patrick Bischop ◽  
Céline Roussel ◽  
Serge Schiffmann ◽  
David Gall
Keyword(s):  
Granule Cell ◽  
Cell Layer ◽  
Cerebellar Granule Cell ◽  
Granule Cell Layer ◽  
Cerebellar Granule ◽  
Morphological Alterations

scholarly journals Immunohistochemical Characterization of Phosphorylated Ubiquitin in the Mouse Hippocampus

2020 ◽  
Author(s):  
Kosuke Kataoka ◽  
Andras Bilkei-Gorzo ◽  
Andreas Zimmer ◽  
Toru Asahi
Keyword(s):  
Cell Layer ◽  
Granule Cell Layer ◽  
Phosphatase And Tensin Homolog ◽  
Neuronal Markers ◽  
Tensin Homolog ◽  
Evolutionarily Conserved ◽  
Previous Hypothesis ◽  
Mouse Hippocampus ◽  
And Function

ABSTRACTMitochondrial autophagy (mitophagy) is an essential and evolutionarily conserved process that maintains mitochondrial integrity via the removal of damaged or superfluous mitochondria in eukaryotic cells. Phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1) and Parkin promote mitophagy and function in a common signaling pathway. PINK1-mediated ubiquitin phosphorylation at Serine 65 (Ser65-pUb) is a key event in the efficient execution of PINK1/Parkin-dependent mitophagy. However, few studies have used immunohistochemistry to analyze Ser65-pUb in the mouse. Here, we examined the immunohistochemical characteristics of Ser65-pUb in the mouse hippocampus. Some hippocampal cells were Ser65-pUb positive, whereas the remaining cells expressed no or low levels of Ser65-pUb. PINK1 deficiency resulted in a decrease in the density of Ser65-pUb-positive cells, consistent with a previous hypothesis based on in vitro research. Interestingly, Ser65-pUb-positive cells were detected in hippocampi lacking PINK1 expression. The CA3 pyramidal cell layer and the dentate gyrus (DG) granule cell layer exhibited significant reductions in the density of Ser65-pUb-positive cells in PINK1-deficient mice. Moreover, Ser65-pUb immunoreactivity colocalized predominantly with neuronal markers. These findings suggest that Ser65-pUb may serve as a biomarker of in situ PINK1 signaling in the mouse hippocampus; however, the results should be interpreted with caution, as PINK1 deficiency downregulated Ser65-pUb only partially.

Cerebellar proteoglycans regulate sonic hedgehog responses during development

Development ◽  
2002 ◽  
Vol 129 (9) ◽  
pp. 2223-2232 ◽  
Author(s):  
Joshua B. Rubin ◽  
Yoojin Choi ◽  
Rosalind A. Segal
Keyword(s):  
Heparan Sulfate ◽  
Sonic Hedgehog ◽  
Granule Cell ◽  
Granule Cells ◽  
Cerebellar Granule Cells ◽  
Cell Layer ◽  
Heparan Sulfate Proteoglycans ◽  
Granule Cell Layer ◽  
Conserved Sequence ◽  
External Granule Cell Layer

Sonic hedgehog promotes proliferation of developing cerebellar granule cells. As sonic hedgehog is expressed in the cerebellum throughout life it is not clear why proliferation occurs only in the early postnatal period and only in the external granule cell layer. We asked whether heparan sulfate proteoglycans might regulate sonic hedgehog-induced proliferation and thereby contribute to the specialized proliferative environment of the external granule cell layer. We identified a conserved sequence within sonic hedgehog that is essential for binding to heparan sulfate proteoglycans, but not for binding to the receptor patched. Sonic hedgehog interactions with heparan sulfate proteoglycans promote maximal proliferation of postnatal day 6 granule cells. By contrast, proliferation of less mature granule cells is not affected by sonic hedgehog-proteoglycan interactions. The importance of proteoglycans for proliferation increases during development in parallel with increasing expression of the glycosyltransferase genes, exostosin 1 and exostosin 2. These data suggest that heparan sulfate proteoglycans, synthesized by exostosins, may be critical determinants of granule cell proliferation.

BDNF stimulates migration of cerebellar granule cells

Development ◽  
2002 ◽  
Vol 129 (6) ◽  
pp. 1435-1442 ◽  
Author(s):  
Paul R. Borghesani ◽  
Jean Michel Peyrin ◽  
Robyn Klein ◽  
Joshua Rubin ◽  
Alexandre R. Carter ◽  
...  
Keyword(s):  
Granule Cell ◽  
Granule Cells ◽  
Cerebellar Granule Cells ◽  
Cell Layer ◽  
Time Lapse ◽  
Granule Cell Layer ◽  
Boyden Chamber ◽  
Cerebellar Granule ◽  
Proliferative Zone ◽  
On Line

During development of the nervous system, neural progenitors arise in proliferative zones, then exit the cell cycle and migrate away from these zones. Here we show that migration of cerebellar granule cells out of their proliferative zone, the external granule cell layer (EGL), is impaired in Bdnf–/– mice. The reason for impaired migration is that BDNF directly and acutely stimulates granule cell migration. Purified Bdnf–/– granule cells show defects in initiation of migration along glial fibers and in Boyden chamber assays. This phenotype can be rescued by exogenous BDNF. Using time-lapse video microscopy we find that BDNF is acutely motogenic as it stimulates migration of individual granule cells immediately after addition. The stimulation of migration reflects both a chemokinetic and chemotactic effect of BDNF. Collectively, these data demonstrate that BDNF is directly motogenic for granule cells and provides a directional cue promoting migration from the EGL to the internal granule cell layer (IGL). Movies available on-line

Dentate Gyrus Immaturity in Schizophrenia

2019 ◽  
Vol 25 (6) ◽  
pp. 528-547 ◽  
Author(s):  
Ayda Tavitian ◽  
Wei Song ◽  
Hyman M. Schipper
Keyword(s):  
Animal Models ◽  
Dentate Gyrus ◽  
Granule Cell ◽  
Cell Layer ◽  
Current Theory ◽  
Position Paper ◽  
Granule Cell Layer ◽  
Molecular Profile ◽  
Rodent Models

Hippocampal abnormalities have been heavily implicated in the pathophysiology of schizophrenia. The dentate gyrus of the hippocampus was shown to manifest an immature molecular profile in schizophrenia subjects, as well as in various animal models of the disorder. In this position paper, we advance a hypothesis that this immature molecular profile is accompanied by an identifiable immature morphology of the dentate gyrus granule cell layer. We adduce evidence for arrested maturation of the dentate gyrus in the human schizophrenia-affected brain, as well as multiple rodent models of the disease. Implications of this neurohistopathological signature for current theory regarding the development of schizophrenia are discussed.

scholarly journals 0420 Fibre-Specific White Matter Neurodegeneration is Associated with Long Sleep Duration After Stroke

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A161-A161
Author(s):  
E W Gottlieb ◽  
N Egorova ◽  
M S Khlif ◽  
W Khan ◽  
E Werden ◽  
...  
Keyword(s):  
White Matter ◽  
Sleep Duration ◽  
Research Council ◽  
Intracranial Volume ◽  
Whole Brain ◽  
Post Stroke ◽  
Echoplanar Imaging ◽  
Long Sleep ◽  
Normal Sleep ◽  
The Brain

Abstract Introduction Long sleep duration in aging populations has recently been proposed as a key modifiable risk factor and sequela of stroke. It is unclear whether the pathogenesis of post-stroke sleep-wake dysfunction is due to focal infarction to regional sleep-wake hubs in the brain, or to accelerated whole-brain neurodegeneration. We utilise a novel technique known as whole-brain fixel-based analyses (FBA) to characterize the first fibre-specific white-matter markers of long sleep duration after stroke. Methods We included 98 radiologically-confirmed ischemic stroke participants (67 male; mean age = 68) and 40 age-matched controls with no history of neurodegenerative disease imaged 3-months post-stroke. Sleep-wake was measured for one week using BodyMedia’s SenseWear armband. Diffusion-weighted MRI (DWI) were acquired using echoplanar imaging and preprocessed using MRtrix3. FBA were employed to identify tracts with altered white-matter fibre-density and fibre-bundle cross-section (FDC) in the long sleep duration (>8 hr, n=20) and normal sleep duration groups (between >6 hr and <8 hr, n=59) compared to controls. Statistical comparisons of FDC between groups were performed at each FDC fixel by a general linear model controlling for age, sex, and intracranial volume. Results Stroke participants with long sleep duration exhibited significant FDC reductions of up to 40% within the cortico-ponto-cerebellar tract when compared to healthy controls (family-wise-error-corrected p=<0.05). Bilateral pontine degeneration was observed at the decussation of the superior cerebellar peduncles. Stroke participants with normal sleep duration exhibited diffuse whole-brain degeneration most apparent along the corpus collosum and cingulum; however, the distribution was less extensive relative to long sleepers (i.e., no cortico-cerebellar projections) and percentage effect reductions did not exceed 20%. Conclusion Long sleep duration after stroke is associated with cortico-ponto-cerebellar degeneration when compared to controls or stroke-participants with normal sleep duration. Excessively long sleep may contribute to post-stroke neurodegeneration beyond the effects of direct infarction and may be a modifiable pharmacological target for abating brain volume loss after stroke. Support This work was supported by the National Health and Medical Research Council project grant (APP1020526), the Brain Foundation, Wicking Trust, Collie-Trust, and Sidney and Fiona Myer Family Foundation. NE was supported by the Australian Research Council DECRA award DE180100893.

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