scholarly journals Investigation of reactive astrogliosis effect on post-stroke cognitive impairment

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Kuo-Lun Huang ◽  
Ing-Tsung Hsiao ◽  
Meng-Yang Ho ◽  
Jung-Lung Hsu ◽  
Yeu-Jhy Chang ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Cortical Atrophy ◽  
Signal Distribution ◽  
Reactive Astrogliosis ◽  
Post Stroke ◽  
Positron Emission ◽  
Path Analyses ◽  
Neurocognitive Evaluation ◽  
Sum Scores ◽  
Left Hemisphere Stroke

Abstract Background The aim of this study is to investigate the associations between post-stroke cognitive impairment (PSCI) severity and reactive astrogliosis (RA) extent on normalized 18F-THK-5351 positron-emission tomography (PET) imaging in amyloid-negative patients with first-ever stroke. Methods We prospectively enrolled 63 amyloid-negative patients with first-ever stroke. Neurocognitive evaluation, MRI, 18F-THK-5351, and 18F-florbetapir PET were performed around 3 months after stroke. The 18F-THK-5351 uptake intensity was normalized using a signal distribution template to obtain the Z-SUM scores as the RA extent in the whole brain and cerebral hemisphere ipsilateral to stroke lesion. We evaluated stroke volume, leukoaraiosis, and brain atrophy on MRI. We used a comprehensive neurocognitive battery to obtain composite cognitive scores, and defined PSCI as a general cognitive function score < − 1. We analyzed the influence of Z-SUM scores on PSCI severity after adjusting for demographic, vascular, and neurodegenerative variables. Results Twenty-five of 63 stroke patients had PSCI. Patients with PSCI had older age, lower education, and more severe cortical atrophy and total Z-SUM scores. Total Z-SUM scores were significantly associated with general cognitive and executive functions at multiple regression models. Path analyses showed that stroke can exert cognitive influence directly by stroke itself as well as indirectly through RA, including total and ipsilateral Z-SUM scores, in patients with either right or left hemisphere stroke. Conclusion The patterns and intensity of 18F-THK-5351 uptake in amyloid-negative patients with first-ever stroke were associated with PSCI manifestations, which suggests that RA presents a modulating effect in PSCI development.

scholarly journals No evidence for amyloid pathology as a key mediator of neurodegeneration post-stroke - a seven year follow-up study

2020 ◽  
Author(s):  
Guri Hagberg ◽  
Hege Ihle-Hansen ◽  
Brynjar Fure ◽  
Bente Thommessen ◽  
Håkon Ihle-Hansen ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Status ◽  
Cortical Atrophy ◽  
Csf Biomarkers ◽  
Stroke Survivors ◽  
Amyloid Β Peptide ◽  
Post Stroke ◽  
Amyloid Pathology ◽  
One Year

Abstract Background Cognitive impairment (CI) with mixed vascular and neurodegenerative pathologies after stroke is common. The role of amyloid pathology in post-stroke CI is unclear. We hypothesize that amyloid deposition, measured with Flutemetamol ( 18 F-Flut) positron emission tomography (PET), is common in 7-year stroke survivors diagnosed with CI and, further, that quantitatively assessed 18 F-Flut-PET uptake after seven years correlates with amyloid-β peptide (Aβ 42 ) levels in cerebrospinal fluid (CSF) at one year, and with measures of neurodegeneration and cognition at seven years post-stroke. Methods 208 patients with first-ever stroke or TIA without pre-existing CI were included during 2007 and 2008. At one- and seven-years post-stroke, cognitive status was assessed, and categorized into dementia, mild cognitive impairment or none. Etiologic sub-classification was based on magnetic resonance imaging (MRI) findings, CSF biomarkers and clinical cognitive profile. At seven years, patients were offered 18 F-Flut-PET, and amyloid-positivity was assessed visually and semi-quantitatively. The associations between 18 F-Flut-PET standardized uptake value ratios (SUVr) and measures of neurodegeneration (medial temporal lobe atrophy (MTLA), global cortical atrophy (GCA)) and cognition (Mini-Mental State Exam (MMSE), Trail-making test A (TMT-A)) and CSF Aβ 42 levels were assessed using linear regression. Results In all, 111 patients completed 7-year follow-up, and 26 patients agreed to PET imaging, of whom 13 had CSF biomarkers from one year. Thirteen out of 26 patients were diagnosed with CI seven years post-stroke, but only one had visually assessed amyloid positivity. CSF Aβ 42 levels at one year, MTA grade, GCA scale, MMSE score or TMT-A at seven years did not correlate with 18 F-Flut-PET SUVr in this cohort. Conclusions Amyloid binding were not common in 7-year stroke survivors diagnosed with CI. Quantitatively assessed amyloid did not correlate with other measures related to neurodegeneration and cognition. Therefore amyloid pathology may not be a key mediator of neurodegeneration seven years post-stroke.

scholarly journals No evidence for amyloid pathology as a key mediator of neurodegeneration post-stroke - a seven year follow-up study

2020 ◽  
Author(s):  
Guri Hagberg ◽  
Hege Ihle-Hansen ◽  
Brynjar Fure ◽  
Bente Thommessen ◽  
Håkon Ihle-Hansen ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Status ◽  
Amyloid Deposition ◽  
Cortical Atrophy ◽  
Csf Biomarkers ◽  
Stroke Survivors ◽  
Post Stroke ◽  
Amyloid Pathology ◽  
One Year

Abstract Background: Cognitive impairment (CI) with mixed vascular and neurodegenerative pathologies after stroke is common. The role of amyloid pathology in post-stroke CI is unclear. We hypothesize that amyloid deposition, measured with Flutemetamol (18F-Flut) positron emission tomography (PET), is common in 7-year stroke survivors diagnosed with CI and, further, that quantitatively assessed 18F-Flut-PET uptake after seven years correlates with amyloid-β peptide (Aβ₄₂) levels in cerebrospinal fluid (CSF) at one year, and with measures of neurodegeneration and cognition at seven years post-stroke. Methods: 208 patients with first-ever stroke or transient Ischemic Attack (TIA) without pre-existing CI were included during 2007 and 2008. At one- and seven-years post-stroke, cognitive status was assessed, and categorized into dementia, mild cognitive impairment or normal. Etiologic sub-classification was based on magnetic resonance imaging (MRI) findings, CSF biomarkers and clinical cognitive profile. At seven years, patients were offered 18F-Flut-PET, and amyloid-positivity was assessed visually and semi-quantitatively. The associations between 18F-Flut-PET standardized uptake value ratios (SUVr) and measures of neurodegeneration (medial temporal lobe atrophy (MTLA), global cortical atrophy (GCA)) and cognition (Mini-Mental State Exam (MMSE), Trail-making test A (TMT-A)) and CSF Aβ₄₂ levels were assessed using linear regression. Results: In total, 111 patients completed 7-year follow-up, and 26 patients agreed to PET imaging, of whom 13 had CSF biomarkers from one year. Thirteen out of 26 patients were diagnosed with CI seven years post-stroke, but only one had visually assessed amyloid positivity. CSF Aβ₄₂ levels at one year, MTA grade, GCA scale, MMSE score or TMT-A at seven years did not correlate with 18F-Flut-PET SUVr in this cohort.Conclusions: Amyloid binding was not common in 7-year stroke survivors diagnosed with CI. Quantitatively assessed, cortical amyloid deposition did not correlate with other measures related to neurodegeneration or cognition. Therefore amyloid pathology may not be a key mediator of neurodegeneration seven years post-stroke.Trial registration: Clinicaltrials.gov (NCT00506818)

scholarly journals No evidence for amyloid pathology as a key mediator of neurodegeneration post-stroke - a seven-year follow-up study

2020 ◽  
Author(s):  
Guri Hagberg ◽  
Hege Ihle-Hansen ◽  
Brynjar Fure ◽  
Bente Thommessen ◽  
Håkon Ihle-Hansen ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Amyloid Deposition ◽  
Trial Registration ◽  
Cortical Atrophy ◽  
Csf Biomarkers ◽  
Stroke Survivors ◽  
Post Stroke ◽  
Amyloid Pathology ◽  
One Year

Abstract Background: Cognitive impairment (CI) with mixed vascular and neurodegenerative pathologies after stroke is common. The role of amyloid pathology in post-stroke CI is unclear. We hypothesize that amyloid deposition, measured with Flutemetamol (18F-Flut) positron emission tomography (PET), is common in seven-year stroke survivors diagnosed with CI and, further, that quantitatively assessed 18F-Flut-PET uptake after seven years correlates with amyloid-β peptide (Aβ₄₂) levels in cerebrospinal fluid (CSF) at one year, and with measures of neurodegeneration and cognition at seven years post-stroke. Methods: 208 patients with first-ever stroke or transient Ischemic Attack (TIA) without pre-existing CI were included during 2007 and 2008. At one- and seven-years post-stroke, cognitive status was assessed, and categorized into dementia, mild cognitive impairment or normal. Etiologic sub-classification was based on magnetic resonance imaging (MRI) findings, CSF biomarkers and clinical cognitive profile. At seven years, patients were offered 18F-Flut-PET, and amyloid-positivity was assessed visually and semi-quantitatively. The associations between 18F-Flut-PET standardized uptake value ratios (SUVr) and measures of neurodegeneration (medial temporal lobe atrophy (MTLA), global cortical atrophy (GCA)) and cognition (Mini-Mental State Exam (MMSE), Trail-making test A (TMT-A)) and CSF Aβ₄₂ levels were assessed using linear regression. Results: In total, 111 patients completed 7-year follow-up, and 26 patients agreed to PET imaging, of whom 13 had CSF biomarkers from one year. Thirteen out of 26 patients were diagnosed with CI seven years post-stroke, but only one had visually assessed amyloid positivity. CSF Aβ₄₂ levels at one year, MTA grade, GCA scale, MMSE score or TMT-A at seven years did not correlate with 18F-Flut-PET SUVr in this cohort.Conclusions: Amyloid binding was not common in 7-year stroke survivors diagnosed with CI. Quantitatively assessed, cortical amyloid deposition did not correlate with other measures related to neurodegeneration or cognition. Therefore, amyloid pathology may not be a key mediator of neurodegeneration seven years post-stroke.Trial registration: Clinicaltrials.gov (NCT00506818). July 23, 2007. Inclusion from February 2007, randomization and intervention from May 2007 and trial registration in July 2007.

scholarly journals Association of tau accumulation and atrophy in mild cognitive impairment: a longitudinal study

2020 ◽  
Author(s):  
Gang Xu ◽  
Shuzhan Zheng ◽  
Zhilong Zhu ◽  
Xiaofeng Yu ◽  
Jian Jiang ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Mediation Analysis ◽  
Linear Models ◽  
Parietal Lobe ◽  
Cortical Atrophy ◽  
Middle Temporal ◽  
Positron Emission ◽  
Mri Scans ◽  
Magnetic Resonance Imaging Mri

Abstract Background To examine the patterns of longitudinal tau accumulation and cortical atrophy and their association in patients with mild cognitive impairment (MCI). Methods We collected 23 participants (60-89 years old, 11 male/12 female) with MCI from the Alzheimer’s Disease Neuroimaging Initiative database. All participants underwent 18 F flortauirpir (FTP) positron emission tomography (PET) and structural magnetic resonance imaging (MRI) scans at the baseline and follow-up visits (12-36 months). General linear models with covariates (baseline age, sex) were used to detect brain areas of significant tau accumulation and atrophy over time. The mediation analysis was employed to explore the potential reason for sequential biomarker changes in MCI progression, adjusting for baseline age, sex, education.Results Voxelwise tau accumulation in MCI patients was predominantly located in inferior temporal, middle temporal, parietal cortex, posterior cingulate, precuneus as well as temporo-parietal regions ( P < 0.001), and MRI atrophy included inferior-middle temporal, parietal lobe, cerebellum and precuneus ( P < 0.001). Longitudinal FTP accumulation was moderately associated with MRI cortical atrophy ( r = 0.409, 95% CI: 0.405-0.414, P < 0.01). Regional analyses indicated significant bivariate associations between MRI cortical atrophy and FTP accumulation (baseline FTP cortical uptake and longitudinal FTP change). The result of the mediation analysis showed the relationship between baseline FTP uptake and longitudinal cortical atrophy was partly mediated by the longitudinal FTP cortical change (indirect effect: 0.0107, P = 0.04).Conclusions Our finding provides a preliminary description of the patterns of longitudinal FTP accumulation and cortical atrophy in MCI progression, and MCI patients with high tau binding level show increase risk of longitudinal tau accumulation, atrophy and cognitive decline.

scholarly journals 18F-Flutemetamol PET post-stroke - a seven year follow-up study

2019 ◽  
Author(s):  
Guri Hagberg ◽  
Hege Ihle-Hansen ◽  
Brynjar Fure ◽  
Bente Thommessen ◽  
Håkon Ihle-Hansen ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Status ◽  
Cortical Atrophy ◽  
Csf Biomarkers ◽  
Stroke Survivors ◽  
Amyloid Β Peptide ◽  
Post Stroke ◽  
Amyloid Pathology ◽  
One Year

Abstract Background: Cognitive impairment (CI) with mixed vascular and neurodegenerative pathologies after stroke is common. The role of amyloid pathology in post-stroke CI is unclear. We hypothesize that amyloid deposition, measured with Flutemetamol (18F-Flut) positron emission tomography (PET), is common in 7-year stroke survivors diagnosed with CI and, further, that quantitatively assessed 18F-Flut-PET uptake after seven years correlates with amyloid-β peptide (Aβ₄₂) levels in cerebrospinal fluid (CSF) at one year, and with measures of neurodegeneration and cognition at seven years post-stroke. Methods: 208 patients with first-ever stroke or TIA without pre-existing CI were included during 2007 and 2008. At one- and seven-years post-stroke, cognitive status was assessed, and categorized into dementia, mild cognitive impairment or none. Etiologic sub-classification was based on magnetic resonance imaging (MRI) findings, CSF biomarkers and clinical cognitive profile. At seven years, patients were offered 18F-Flut-PET, and amyloid-positivity was assessed visually and semi-quantitatively. The associations between 18F-Flut-PET standardized uptake value ratios (SUVr) and measures of neurodegeneration (medial temporal lobe atrophy (MTLA), global cortical atrophy (GCA)) and cognition (Mini-Mental State Exam (MMSE), Trail-making test A (TMT-A)) and CSF Aβ₄₂ levels were assessed using linear regression. Results: In all, 111 patients completed 7-year follow-up, and 26 patients agreed to PET imaging, of whom 13 had CSF biomarkers from one year. Thirteen out of 26 patients were diagnosed with CI seven years post-stroke, but only one had visually assessed amyloid positivity. CSF Aβ₄₂ levels at one year, MTA grade, GCA scale, MMSE score or TMT-A at seven years did not correlate with 18F-Flut-PET SUVr in this cohort.Conclusions: Amyloid binding were not common in 7-year stroke survivors diagnosed with CI. Quantitatively assessed amyloid did not correlate with other measures related to neurodegeneration and cognition. Therefore amyloid pathology may not be a key mediator of neurodegeneration seven years post-stroke.

Brain FDG PET for the Etiological Diagnosis of Clinically Uncertain Cognitive Impairment During Delirium in Remission

2020 ◽  
Vol 77 (4) ◽  
pp. 1609-1622
Author(s):  
Franziska Mathies ◽  
Catharina Lange ◽  
Anja Mäurer ◽  
Ivayla Apostolova ◽  
Susanne Klutmann ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Fdg Pet ◽  
False Negative ◽  
Ground Truth ◽  
Etiological Diagnosis ◽  
Geriatric Unit ◽  
Positron Emission ◽  
The Brain ◽  
Hospitalized Geriatric Patients

Background: Positron emission tomography (PET) of the brain with 2-[F-18]-fluoro-2-deoxy-D-glucose (FDG) is widely used for the etiological diagnosis of clinically uncertain cognitive impairment (CUCI). Acute full-blown delirium can cause reversible alterations of FDG uptake that mimic neurodegenerative disease. Objective: This study tested whether delirium in remission affects the performance of FDG PET for differentiation between neurodegenerative and non-neurodegenerative etiology of CUCI. Methods: The study included 88 patients (82.0±5.7 y) with newly detected CUCI during hospitalization in a geriatric unit. Twenty-seven (31%) of the patients were diagnosed with delirium during their current hospital stay, which, however, at time of enrollment was in remission so that delirium was not considered the primary cause of the CUCI. Cases were categorized as neurodegenerative or non-neurodegenerative etiology based on visual inspection of FDG PET. The diagnosis at clinical follow-up after ≥12 months served as ground truth to evaluate the diagnostic performance of FDG PET. Results: FDG PET was categorized as neurodegenerative in 51 (58%) of the patients. Follow-up after 16±3 months was obtained in 68 (77%) of the patients. The clinical follow-up diagnosis confirmed the FDG PET-based categorization in 60 patients (88%, 4 false negative and 4 false positive cases with respect to detection of neurodegeneration). The fraction of correct PET-based categorization did not differ between patients with delirium in remission and patients without delirium (86% versus 89%, p = 0.666). Conclusion: Brain FDG PET is useful for the etiological diagnosis of CUCI in hospitalized geriatric patients, as well as in patients with delirium in remission.

scholarly journals Post-stroke cognitive impairment on the Mini-Mental State Examination primarily relates to left middle cerebral artery infarcts

2021 ◽  
pp. 174749302098455
Author(s):  
Nick A Weaver ◽  
Angelina K Kancheva ◽  
Jae-Sung Lim ◽  
J Matthijs Biesbroek ◽  
Irene MC Huenges Wajer ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Cognitive Deficits ◽  
Mini Mental State Examination ◽  
Left Middle Cerebral Artery ◽  
Post Stroke ◽  
Lesion Symptom Mapping ◽  
State Examination ◽  
Left Middle

Background Post-stroke cognitive impairment can occur after damage to various brain regions, and cognitive deficits depend on infarct location. The Mini-Mental State Examination (MMSE) is still widely used to assess post-stroke cognition, but it has been criticized for capturing only certain cognitive deficits. Along these lines, it might be hypothesized that cognitive deficits as measured with the MMSE primarily involve certain infarct locations. Aims This comprehensive lesion-symptom mapping study aimed to determine which acute infarct locations are associated with post-stroke cognitive impairment on the MMSE. Methods We examined associations between impairment on the MMSE (<5th percentile; normative data) and infarct location in 1198 patients (age 67 ± 12 years, 43% female) with acute ischemic stroke using voxel-based lesion-symptom mapping. As a frame of reference, infarct patterns associated with impairments in individual cognitive domains were determined, based on a more detailed neuropsychological assessment. Results Impairment on the MMSE was present in 420 patients (35%). Large voxel clusters in the left middle cerebral artery territory and thalamus were significantly (p < 0.01) associated with cognitive impairment on the MMSE, with highest odds ratios (>15) in the thalamus and superior temporal gyrus. In comparison, domain-specific impairments were related to various infarct patterns across both hemispheres including the left medial temporal lobe (verbal memory) and right parietal lobe (visuospatial functioning). Conclusions Our findings indicate that post-stroke cognitive impairment on the MMSE primarily relates to infarct locations in the left middle cerebral artery territory. The MMSE is apparently less sensitive to cognitive deficits that specifically relate to other locations.

Post-stroke Cognitive Impairment and Malnutrition in the Elderly (PCIME): study design and protocol

2021 ◽  
Author(s):  
Zahra Vahabi ◽  
M. Reza Azarpazhooh ◽  
Shima Raeesi ◽  
Shahram Oveisgharan ◽  
Farnaz Etesam ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Study Design ◽  
The Elderly ◽  
Post Stroke
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