Hippocampal atrophy correlates with the severity of cognitive decline

2006 ◽  
Vol 19 (4) ◽  
pp. 767-777 ◽  
Author(s):  
Burcu Balam Yavuz ◽  
Servet Ariogul ◽  
Mustafa Cankurtaran ◽  
Kader Karli Oguz ◽  
Meltem Halil ◽  
...  
Keyword(s):  
Regression Analysis ◽  
Cognitive Impairment ◽  
Early Diagnosis ◽  
Cognitive Decline ◽  
Multivariate Regression Analysis ◽  
Hippocampal Volume ◽  
Cognitive Status ◽  
Hippocampal Atrophy ◽  
Covariate Effects ◽  
Left Hippocampus

Background: The aim of this study is to compare the results of magnetic resonance (MR) imaging, particularly the decline in hippocampal volume, of patients with Alzheimer's disease (AD) and mild cognitive impairment (MCI) with healthy age-matched controls, to examine the reliability of hippocampal volumetry in the early diagnosis of AD and the correlation of the severity of hippocampal atrophy with the severity of cognitive decline.Methods: Twenty-six AD, 22 MCI and 15 normal cognitive status (NCS) patients were scanned with a 3 Tesla MR scanner. Hippocampus volumes were detected manually by Osiris 4.18.Results: Multivariate regression analysis, which was performed to adjust the covariate effects of education, age, gender, hypertension and diabetes mellitus, showed that hippocampal atrophy was correlated with AD and MCI for right hippocampus; AD, MCI and age for left hippocampus independent of other parameters. A second regression analysis revealed that MMSE was correlated with hippocampal volume.Conclusions: Hippocampal volumetry can be used in early diagnosis of cognitive impairment, as well as grading cognitive decline.

scholarly journals Increased Serum Neuropeptide Galanin Level Is a Predictor of Cognitive Dysfunction in Patients with Hip Fracture

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Zichao Xue ◽  
Ke Zhang ◽  
Biao Luo ◽  
Long Fan ◽  
Ruizhe Zhao ◽  
...  
Keyword(s):  
Regression Analysis ◽  
Cognitive Impairment ◽  
Hip Fracture ◽  
Cognitive Decline ◽  
Cognitive Dysfunction ◽  
Large Scale ◽  
Linear Regression Analysis ◽  
Cognitive Status ◽  
Significant Independent Predictor ◽  
Cognitively Normal

Background. Hip fracture is a common occurrence in elderly populations and is frequently followed by various levels of cognitive dysfunction, leading to adverse functional outcomes. Risk stratification of hip fracture patients to identify high-risk subsets can enable improved strategies to mitigate cognitive complications. The neuropeptide galanin has multiple neurological functions, and altered levels are documented in dementia-type and depression disorders. The present study investigated the association of serum neuropeptide galanin levels in hip fracture patients with the occurrence of cognitive dysfunction during the first week of admission. Methods. 276 hip fracture patients without preexisting delirium, cognitive impairment, or severe mental disorders were included in a cross-sectional study. Serum galanin levels were assessed by ELISA on the second day of admission. Routine clinical and laboratory variables were documented. MoCA was performed within 1 week, and those with a score < 26 were categorized with “cognitive decline.” Inferential statistics including multiple linear regression analysis were applied to determine the association of serum galanin level and cognitive status. Results. 141 patients were categorized with “cognitive decline,” and 135 patients were categorized as “cognitively normal.” Serum galanin was highly significantly increased in the “cognitive decline” group ( 34.2 ± 4.8 , pg/ml) compared to the “cognitively normal” group ( 28.9 ± 3.7 , pg/ml) and showed significant negative correlation with MoCA scores ( r = − 0.229 , p = 0.016 ). Regression analysis showed serum galanin as the sole significant independent predictor of lower MoCA scores ( β = 0.231 , p = 0.035 ) while age, gender, blood pressure, cholesterol, and blood glucose levels had no significant association. Conclusion. Higher serum galanin predicted the development of cognitive dysfunction and worse MoCA scores in a cohort of hip fracture patients without preexisting cognitive impairment or delirium at admission, thus warranting large-scale studies investigating galanin as a candidate biomarker to identify hip fracture patients at risk of cognitive decline.

scholarly journals The Effect of CAG Repeats within the Non-Pathological Range in the HTT Gene on Cognitive Functions in Patients with Subjective Cognitive Decline and Mild Cognitive Impairment

Diagnostics ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1051
Author(s):  
Valentina Bessi ◽  
Salvatore Mazzeo ◽  
Silvia Bagnoli ◽  
Giulia Giacomucci ◽  
Assunta Ingannato ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Cognitive Decline ◽  
Spatial Ability ◽  
Cognitive Status ◽  
Cag Repeat ◽  
Cag Repeats ◽  
Subjective Cognitive Decline ◽  
Visual Spatial ◽  
Premorbid Intelligence

The Huntingtin gene (HTT) is within a class of genes containing a key region of CAG repeats. When expanded beyond 39 repeats, Huntington disease (HD) develops. Individuals with less than 35 repeats are not associated with HD. Increasing evidence has suggested that CAG repeats play a role in modulating brain development and brain function. However, very few studies have investigated the effect of CAG repeats in the non-pathological range on cognitive performances in non-demented individuals. In this study, we aimed to test how CAG repeats’ length influences neuropsychological scores in patients with subjective cognitive decline (SCD) and mild cognitive impairment (MCI). We included 75 patients (46 SCD and 29 MCI). All patients underwent an extensive neuropsychological battery and analysis of HTT alleles to quantify the number of CAG repeats. Results: CAG repeat number was positively correlated with scores of tests assessing for executive function, visual–spatial ability, and memory in SCD patients, while in MCI patients, it was inversely correlated with scores of visual–spatial ability and premorbid intelligence. When we performed a multiple regression analysis, we found that these relationships still remained, also when adjusting for possible confounding factors. Interestingly, logarithmic models better described the associations between CAG repeats and neuropsychological scores. CAG repeats in the HTT gene within the non-pathological range influenced neuropsychological performances depending on global cognitive status. The logarithmic model suggested that the positive effect of CAG repeats in SCD patients decreases as the number of repeats grows.

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 Health Trajectories in Swedish Centenarians

2020 ◽  
Vol 76 (1) ◽  
pp. 157-163
Author(s):  
Davide L Vetrano ◽  
Giulia Grande ◽  
Alessandra Marengoni ◽  
Amaia Calderón-Larrañaga ◽  
Debora Rizzuto
Keyword(s):  
Older Adults ◽  
Cognitive Impairment ◽  
Cognitive Decline ◽  
Chronic Diseases ◽  
Care Delivery ◽  
Cognitive Status ◽  
National Study ◽  
Health Trajectories ◽  
Kungsholmen Project ◽  
Cognitively Intact

Abstract Background Longitudinal studies describing centenarians’ health trajectories are currently lacking. We compared health trajectories of older adults becoming centenarians and their shorter-living counterparts in terms of chronic diseases, disability, and cognitive decline. Methods We identified 3,573 individuals participating in the Kungsholmen Project and the Swedish National Study on Aging and Care in Kungsholmen who lived &lt;100 years and 222 who survived to their 100th birthday. Trajectories of chronic diseases, disability (impaired activities of daily living), and cognitive status were obtained via linear mixed models over 13 years. Results Centenarians had fewer chronic diseases than noncentenarians. Before age 85, centenarians showed slower health changes. In centenarians, multimorbidity, disability, and cognitive impairment occurred 4 to 9 years later than in noncentenarians. After age 85, the speed of accumulation of chronic diseases, disabilities, and cognitive decline accelerated in centenarians. At age 100, 39% of the centenarians were cognitively intact and 55% had escaped disability. Only 5% were free of multimorbidity at age 100. When compared with their shorter lived counterparts, in terms of years spent in poor health, centenarians experienced more years with multimorbidity (9.4 vs 6.8 years; p &lt; .001), disability (4.3 vs 3.1 years; p = .005), and cognitive impairment (6.3 vs 4.3 years; p &lt; .001). Conclusions Older people who become centenarians present a delay in the onset of morbidity, but spend more years in this condition compared to their shorter lived peers. The observation of older adults’ health trajectories might help to forecast healthier aging, and plan future medical and social care delivery.

scholarly journals Role of HMGB1 in an Animal Model of Vascular Cognitive Impairment Induced by Chronic Cerebral Hypoperfusion

2020 ◽  
Vol 21 (6) ◽  
pp. 2176 ◽  
Author(s):  
Amelia Nur Vidyanti ◽  
Jia-Yu Hsieh ◽  
Kun-Ju Lin ◽  
Yao-Ching Fang ◽  
Ismail Setyopranoto ◽  
...  
Keyword(s):  
Animal Model ◽  
Cognitive Impairment ◽  
Cognitive Decline ◽  
Chronic Phase ◽  
Vascular Cognitive Impairment ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Hippocampal Atrophy ◽  
Tnf Α

The pathophysiology of vascular cognitive impairment (VCI) is associated with chronic cerebral hypoperfusion (CCH). Increased high-mobility group box protein 1 (HMGB1), a nonhistone protein involved in injury and inflammation, has been established in the acute phase of CCH. However, the role of HMGB1 in the chronic phase of CCH remains unclear. We developed a novel animal model of CCH with a modified bilateral common carotid artery occlusion (BCCAO) in C57BL/6 mice. Cerebral blood flow (CBF) reduction, the expression of HMGB1 and its proinflammatory cytokines (tumor necrosis factor-alpha [TNF-α], interleukin [IL]-1β, and IL-6), and brain pathology were assessed. Furthermore, we evaluated the effect of HMGB1 suppression through bilateral intrahippocampus injection with the CRISPR/Cas9 knockout plasmid. Three months after CCH induction, CBF decreased to 30–50% with significant cognitive decline in BCCAO mice. The 7T-aMRI showed hippocampal atrophy, but amyloid positron imaging tomography showed nonsignificant amyloid-beta accumulation. Increased levels of HMGB1, TNF-α, IL-1β, and IL-6 were observed 3 months after BCCAO. HMGB1 suppression with CRISPR/Cas9 knockout plasmid restored TNF-α, IL-1β, and IL-6 and attenuated hippocampal atrophy and cognitive decline. We believe that HMGB1 plays a pivotal role in CCH-induced VCI pathophysiology and can be a potential therapeutic target of VCI.

Dysregulation of Hypothalamic-Pituitary-Adrenal Axis Explain the Dynamic Association Between Glucose Fluctuation and Cognitive

2020 ◽  
Vol 10 (2) ◽  
pp. 477-483
Author(s):  
Peng Wenfang ◽  
Shen Lisha ◽  
Xia Lili ◽  
Tang Yubing ◽  
Li Huihua ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Regression Analysis ◽  
Cognitive Impairment ◽  
Hpa Axis ◽  
Multivariate Regression ◽  
Multivariate Regression Analysis ◽  
Glucose Fluctuation

Objective—Type 2 diabetes mellitus is a risk factor for cognitive dysfunction. However, the underlying mechanism of cognitive decline in patients with type 2 diabetes mellitus is still elusive. Dysregulation of HPA axis is related to cognitive impairment. The present study aims to calculate explanation of the association between glucose fluctuation and cognitive function by HPA axis in type 2 diabetes mellitus patients. Methods—The mean amplitude of glycemic excursion (MAGE) was analyzed by a continuous glucose monitoring system (CGMS) for 3 days in 330 elderly type 2 diabetes mellitus patients. All the subjects received a set of neuropsychological test battery for cognitive assessment. The diurnal rhythm of cortisol was also analyzed. Linear multivariate regression analysis was performed to explore the relationship between glucose fluctuation, cortisol parameters and cognitive parameters. Results—MAGE was observed to be associated with diurnal cortisol fall but with neither cortisol awakening response (CAR) nor overall mean cortisol levels (t = –2.195, P = 0.030). Linear multivariate regression analysis displayed that MAGE and average diurnal cortisol fall were uniquely associated with some cognitive parameters, such as AVLT trial, FAS, and TMT (P < 0.05). Conclusion—Glucose fluctuation was strongly associated with cognitive impairment in elderly type 2 diabetes mellitus patients. Especially in executive function, attention and processing speed. Dysregulation of HPA axis was probably the cause of cognitive dysfunction in these patients.

scholarly journals Dissociable influences of APOE ε4 and polygenic risk of AD dementia on amyloid and cognition

Neurology ◽  
2018 ◽  
Vol 90 (18) ◽  
pp. e1605-e1612 ◽  
Author(s):  
Tian Ge ◽  
Mert R. Sabuncu ◽  
Jordan W. Smoller ◽  
Reisa A. Sperling ◽  
Elizabeth C. Mormino ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Genetic Risk ◽  
Large Scale ◽  
Association Studies ◽  
Specific Effect ◽  
Hippocampal Volume ◽  
Risk Scores ◽  
Hippocampal Atrophy ◽  
Genome Wide Association Studies ◽  
Polygenic Risk

ObjectiveTo investigate the effects of genetic risk of Alzheimer disease (AD) dementia in the context of β-amyloid (Aβ) accumulation.MethodsWe analyzed data from 702 participants (221 clinically normal, 367 with mild cognitive impairment, and 114 with AD dementia) with genetic data and florbetapir PET available. A subset of 669 participants additionally had longitudinal MRI scans to assess hippocampal volume. Polygenic risk scores (PRSs) were estimated with summary statistics from previous large-scale genome-wide association studies of AD dementia. We examined relationships between APOE ε4 status and PRS with longitudinal Aβ and cognitive and hippocampal volume measurements.ResultsAPOE ε4 was strongly related to baseline Aβ, whereas only weak associations between PRS and baseline Aβ were present. APOE ε4 was additionally related to greater memory decline and hippocampal atrophy in Aβ+ participants. When APOE ε4 was controlled for, PRS was related to cognitive decline in Aβ+ participants. Finally, PRSs were associated with hippocampal atrophy in Aβ− participants and weakly associated with baseline hippocampal volume in Aβ+ participants.ConclusionsGenetic risk factors of AD dementia demonstrate effects related to Aβ, as well as synergistic interactions with Aβ. The specific effect of faster cognitive decline in Aβ+ individuals with higher genetic risk may explain the large degree of heterogeneity in cognitive trajectories among Aβ+ individuals. Consideration of genetic variants in conjunction with baseline Aβ may improve enrichment strategies for clinical trials targeting Aβ+ individuals most at risk for imminent cognitive decline.

scholarly journals Plasma ceramides are altered in mild cognitive impairment and predict cognitive decline and hippocampal volume loss

2010 ◽  
Vol 6 (5) ◽  
pp. 378-385 ◽  
Author(s):  
Michelle M. Mielke ◽  
Norman J. Haughey ◽  
Veera Venkata Ratnam Bandaru ◽  
Steven Schech ◽  
Richard Carrick ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Cognitive Decline ◽  
Hippocampal Volume ◽  
Volume Loss
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