scholarly journals Longitudinal hippocampal volumetric changes in mice following brain infarction

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Vanessa H. Brait ◽  
David K. Wright ◽  
Mohsen Nategh ◽  
Alexander Oman ◽  
Warda T. Syeda ◽  
...  
Keyword(s):  
Brain Infarction ◽  
Parenchymal Cell ◽  
Vascular Cognitive Impairment ◽  
Hippocampal Volume ◽  
Artery Occlusion ◽  
Hippocampal Atrophy ◽  
Volume Changes ◽  
Post Surgery ◽  
Mri Scans ◽  
Infarcted Tissue

AbstractHippocampal atrophy is increasingly described in many neurodegenerative syndromes in humans, including stroke and vascular cognitive impairment. However, the progression of brain volume changes after stroke in rodent models is poorly characterized. We aimed to monitor hippocampal atrophy occurring in mice up to 48-weeks post-stroke. Male C57BL/6J mice were subjected to an intraluminal filament-induced middle cerebral artery occlusion (MCAO). At baseline, 3-days, and 1-, 4-, 12-, 24-, 36- and 48-weeks post-surgery, we measured sensorimotor behavior and hippocampal volumes from T2-weighted MRI scans. Hippocampal volume—both ipsilateral and contralateral—increased over the life-span of sham-operated mice. In MCAO-subjected mice, different trajectories of ipsilateral hippocampal volume change were observed dependent on whether the hippocampus contained direct infarction, with a decrease in directly infarcted tissue and an increase in non-infarcted tissue. To further investigate these volume changes, neuronal and glial cell densities were assessed in histological brain sections from the subset of MCAO mice lacking hippocampal infarction. Our findings demonstrate previously uncharacterized changes in hippocampal volume and potentially brain parenchymal cell density up to 48-weeks in both sham- and MCAO-operated mice.

Measurement of hippocampal volume changes in serial MRI scans

1999 ◽  
Author(s):  
Julia A. Schnabel ◽  
Louis Lemieux ◽  
U. C. Wieshmann ◽  
Simon R. Arridge
Keyword(s):  
Hippocampal Volume ◽  
Volume Changes ◽  
Mri Scans ◽  
Serial Mri

Brain Atrophy Rates in Normal Aging and Alzheimer Disease

2017 ◽  
Vol 1 (1) ◽  
pp. 01-02
Author(s):  
Micki Dexte
Keyword(s):  
Clinical Trials ◽  
Alzheimer Disease ◽  
Entorhinal Cortex ◽  
Brain Atrophy ◽  
Hippocampal Volume ◽  
Normal Aging ◽  
Hippocampal Atrophy ◽  
Healthy Controls ◽  
Volume Changes ◽  
Longitudinal Mri

The objectives of this study were to (1) compare atrophy rates associated with normal aging and Alzheimer disease (AD) using the semi-automated Boundary Shift Integral (BSI) method and manual tracing of the entorhinal cortex (ERC) and hippocampus and (2) calculate power of BSI vs. ERC and hippocampal volume changes for clinical trials in AD. We quantified whole brain and ventricular BSI atrophy rates and ERC and hippocampal atrophy rates from longitudinal MRI data in 20 AD patients and 22 age-matched healthy controls.

The Effects of Mean of Visit-to-Visit Blood Pressure on Incident Brain Vascular Lesions and Functional-Cognitive Decline

2021 ◽  
pp. 1-12
Author(s):  
Bibek Gyanwali ◽  
Celestine Xue Ting Cai ◽  
Christopher Chen ◽  
Henri Vrooman ◽  
Chuen Seng Tan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cognitive Decline ◽  
Hippocampal Volume ◽  
Intracranial Stenosis ◽  
Vascular Lesions ◽  
Linear Regression Models ◽  
Volume Functional ◽  
Mri Scans ◽  
The Mean

Background: Cerebrovascular disease (CeVD) is an underlying cause of cognitive impairment and dementia. Hypertension is a known risk factor of CeVD, but the effects of mean of visit-to-visit blood pressure (BP) on incident CeVD and functional-cognitive decline remains unclear. Objective: To determine the association between mean of visit-to-visit BP with the incidence and progression of CeVD [white matter hyperintensities (WMH), infarcts (cortical infarcts and lacunes), cerebral microbleeds (CMBs), intracranial stenosis, and hippocampal volume] as well as functional-cognitive decline over 2 years of follow-up. Methods: 373 patients from a memory-clinic underwent BP measurements at baseline, year 1, and year 2. The mean of visit-to-visit systolic BP, diastolic BP, pulse pressure, and mean arterial pressure were calculated. Baseline and year 2 MRI scans were graded for WMH, infarcts, CMBs, intracranial stenosis, and hippocampal volume. Functional-cognitive decline was assessed using locally validated protocol. Logistic and linear regression models with odds ratios, mean difference, and 95%confidence interval were constructed to analyze associations of visit-to-visit BP on CeVD incidence and progression as well as functional-cognitive decline. Results: Higher mean of visit-to-visit diastolic BP was associated with WMH progression. Higher tertiles of diastolic BP was associated with WMH progression and incident CMBs. There was no association between mean of visit-to-visit BP measures with incident cerebral infarcts, intracranial stenosis, change in hippocampal volume, and functional-cognitive decline. Conclusion: These findings suggest the possibility of hypertension-related vascular brain damage. Careful monitoring and management of BP in elderly patients is essential to reduce the incidence and progression of CeVD.

Neuroanatomical Hippocampal Structures and Heritability of Hippocampal Volume in Relation to Memory

1969 ◽  
Author(s):  
Shaughnelene Smith
Keyword(s):  
Right Hemisphere ◽  
Environmental Control ◽  
Data Bank ◽  
Monozygotic Twin ◽  
Hippocampal Volume ◽  
Brain Images ◽  
Sibling Pairs ◽  
Human Connectome Project ◽  
Mri Scans ◽  
The Right

The goal of this project was to investigate the genetic heritability of hippocampal volume using twin pairs and assess the neuroanatomical structures of the hippocampus and how these properties relate to memory in humans. Data for this project was obtained from the Human Connectome Project: a data bank established to provide neural images to the public. MRI scans were used to obtain brain images of each of the participants and basic cognitive tasks were used to obtain memory ability. To date, 506 subjects have been analyzed: 66 monozygotic twin pairs, 44 dizygotic twin pairs, and 47 sibling pairs. The data collection for of this project was three-fold. First, segmentations were performed to calculate the volume of the anterior and posterior regions of the hippocampus. Secondly, the magnitudes of hippocampus dentations were recorded within the three segments – the head, body, and tail – of the hippocampus. Lastly, visual inspection was used to asses incomplete inversions, which was defined as an atypical anatomical pattern in the hippocampus. The results of this project showed a strong heritability observed on the right anterior hippocampus (hb2=1.365) and right amygdala (hb2=1.315), moderate heritability observed on the left posterior hippocampus (hb2=0.765), and weak heritability observed on the right posterior hippocampus (hb2=0.2654). This indicates that hippocampal volumetric heritability showed strong genetic control for the right hemisphere and strong environmental control for the left hemisphere. The project is still in the process of correlating the anatomical structures to the memory capabilities of the participants. 

scholarly journals Ezetimibe Attenuates Oxidative Stress and Neuroinflammation via the AMPK/Nrf2/TXNIP Pathway after MCAO in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-14 ◽  
Author(s):  
Jing Yu ◽  
Wen-na Wang ◽  
Nathanael Matei ◽  
Xue Li ◽  
Jin-wei Pang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ischemic Stroke ◽  
Brain Infarction ◽  
Neutrophil Infiltration ◽  
Artery Occlusion ◽  
Receptor Protein ◽  
Related Factor ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Interacting Protein

Oxidative stress and neuroinflammation play essential roles in ischemic stroke-induced brain injury. Previous studies have reported that Ezetimibe (Eze) exerts antioxidative stress and anti-inflammatory properties in hepatocytes. In the present study, we investigated the effects of Eze on oxidative stress and neuroinflammation in a rat middle cerebral artery occlusion (MCAO) model. One hundred and ninety-eight male Sprague-Dawley rats were used. Animals assigned to MCAO were given either Eze or its control. To explore the downstream signaling of Eze, the following interventions were given: AMPK inhibitor dorsomorphin and nuclear factor erythroid 2-related factor 2 (Nrf2) siRNA. Intranasal administration of Eze, 1 h post-MCAO, further increased the endogenous p-AMPK expression, reducing brain infarction, neurologic deficits, neutrophil infiltration, microglia/macrophage activation, number of dihydroethidium- (DHE-) positive cells, and malonaldehyde (MDA) levels. Specifically, treatment with Eze increased the expression of p-AMPK, Nrf2, and HO-1; Romo-1, thioredoxin-interacting protein (TXNIP), NOD-like receptor protein 3 (NLRP3), Cleaved Caspase-1, and IL-1β were reduced. Dorsomorphin and Nrf2 siRNA reversed the protective effects of Eze. In summary, Eze decreases oxidative stress and subsequent neuroinflammation via activation of the AMPK/Nrf2/TXNIP pathway after MCAO in rats. Therefore, Eze may be a potential therapeutic approach for ischemic stroke patients.

The role of high-mobility group box protein 1 in chronic cerebral hypoperfusion-induced vascular cognitive impairment animals

2019 ◽  
Author(s):  
Amelia Nur Vidyanti ◽  
Jia-Yu Hsieh ◽  
Kun-Ju Lin ◽  
Yao-Ching Fang ◽  
Ismail Setyopranoto ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Decline ◽  
High Mobility ◽  
Vascular Cognitive Impairment ◽  
High Mobility Group ◽  
Cerebral Hypoperfusion ◽  
Hippocampal Atrophy ◽  
Amyloid Pet ◽  
Knock Out

Abstract Background: The molecular mechanisms of vascular cognitive impairment (VCI) are diverse and still in puzzle. VCI could be attributed to chronic cerebral hypoperfusion (CCH). CCH may cause a cascade of reactions involved in ischemia and neuro-inflammation which plays important roles in the pathophysiology of VCI. High-mobility group box protein 1 (HMGB1) is a non-histone protein that serves as a damage-associated molecular signal leading to cascades of inflammation. Increased level of HMGB1 has been established in the acute phase of CCH. However, the role of HMGB1 at the chronic phase of CCH remains elucidated. Methods: We performed modified bilateral common carotid artery occlusion (BCCAO) in C57BL/6 mice to induce CCH. We examined the cerebral blood flow (CBF) reduction by laser doppler flowmetry, the protein expression of HMGB1 and its pro-inflammatory cytokines (TNF-a, IL-1b, and IL-6) by western blotting and immunohistochemistry. The brain pathology was assessed by 7T-animal MRI and amyloid-b accumulation was assessed by amyloid-PET scanning. We further evaluated the effect of HMGB1 suppression by injecting CRISPR/Cas9 knock-out plasmid intra-hippocampus bilaterally. Results: There were reduction of CBF up to 50% which persisted three months after CCH. The modified-BCCAO animals developed significant cognitive decline. The 7T-MRI image showed hippocampal atrophy, although the amyloid-PET showed no significant amyloid-beta accumulation. Increased protein levels of HMGB1, TNF-a and IL-1b were found three months after BCCAO. HMGB1 suppression by CRISPR/Cas9 knock-out plasmid restored the CBF, IL-1B, TNF-alpha, IL-6, and attenuated hippocampal atrophy and cognitive decline. Conclusion: HMGB1 plays a pivotal role in the pathophysiology of the animal model of CCH and it might be a candidate as therapeutic targets of VCI.

scholarly journals Hippocampal Volume in Provisional Tic Disorder Predicts Tic Severity at 12-Month Follow-up

2020 ◽  
Vol 9 (6) ◽  
pp. 1715
Author(s):  
Soyoung Kim ◽  
Deanna J. Greene ◽  
Carolina Badke D’Andrea ◽  
Emily C. Bihun ◽  
Jonathan M. Koller ◽  
...  
Keyword(s):  
Symptom Severity ◽  
Structural Mri ◽  
Hippocampal Volume ◽  
Subcortical Structures ◽  
Tic Disorder ◽  
Tic Severity ◽  
Mri Scans ◽  
One Year ◽  
Important Marker

Previous studies have investigated differences in the volumes of subcortical structures (e.g., caudate nucleus, putamen, thalamus, amygdala, and hippocampus) between individuals with and without Tourette syndrome (TS), as well as the relationships between these volumes and tic symptom severity. These volumes may also predict clinical outcome in Provisional Tic Disorder (PTD), but that hypothesis has never been tested. This study aimed to examine whether the volumes of subcortical structures measured shortly after tic onset can predict tic symptom severity at one-year post-tic onset, when TS can first be diagnosed. We obtained T1-weighted structural MRI scans from 41 children with PTD (25 with prospective motion correction (vNavs)) whose tics had begun less than 9 months (mean 4.04 months) prior to the first study visit (baseline). We re-examined them at the 12-month anniversary of their first tic (follow-up), assessing tic severity using the Yale Global Tic Severity Scale. We quantified the volumes of subcortical structures using volBrain software. Baseline hippocampal volume was correlated with tic severity at the 12-month follow-up, with a larger hippocampus at baseline predicting worse tic severity at follow-up. The volumes of other subcortical structures did not significantly predict tic severity at follow-up. Hippocampal volume may be an important marker in predicting prognosis in Provisional Tic Disorder.

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