006 Effect of apolipoprotein e ε4 allele on medial temporal lobe atrophy in ischaemic stroke patients

2018 ◽  
Vol 89 (6) ◽  
pp. A4.1-A4
Author(s):  
Mohamed Salah Khlif ◽  
Emilio Werden ◽  
Natalia Egorova ◽  
Wasim Khan ◽  
Amy Brodtmann
Keyword(s):  
Cognitive Impairment ◽  
Ischaemic Stroke ◽  
Temporal Lobe ◽  
Medial Temporal Lobe ◽  
Hippocampal Volume ◽  
Stroke Survivors ◽  
Apoe Ε4 ◽  
Ε4 Allele ◽  
The Right ◽  
Time Point

IntroductionApolipoprotein E (APOE) ε4 allele is a known risk factor for the development of cognitive impairment. APOE ε4 carriers have been reported as having lower hippocampal volume in Alzheimer’s disease, mild cognitive impairment, and in healthy cohorts,1 but this is not well investigated in stroke. Here, we compared the regional volume in the medial temporal lobe in ischaemic stroke survivors, with and without the ε4 allele, three (time point 1, t1) and twelve (t2) months after stroke.Methods21 APOE ε4 carriers and 21 non-carriers, matched for lesion size and location and for neurological impairment as measured by NIHSS, were sampled from the CANVAS study, a longitudinal imaging study in stroke survivors.2 A mixed-effect linear model was used to analyse the effect of the ε4 allele on hippocampal, entorhinal, and para-hippocampal volumes, adjusting for age, sex, years of education, and total intracranial volume. Volumes were estimated using the longitudinal stream in FreeSurfer 5.3.ResultsThe left hippocampal (pt1=0.038, pt2=0.040) and entorhinal (pt1=0.044, pt2=0.038) volumes were significantly lower in the ε4-carrier group at each time point. The right entorhinal (pt1=pt2=0.002) and para-hippocampal (pt1=0.018, pt2=0.020) volumes were also significantly lower in the ε4-carrier group, but there was no difference in the right hippocampal volume (pt1=pt2=0.055) between the two groups. The group-time interaction was significant for the left para-hippocampal cortex (p=0.019): ε4 non-carriers showed a significant volume increase (p=0.018) between t1 and t2.ConclusionThese findings suggest that stroke survivors who carry the APOE-ε4 allele will experience greater atrophy in the medial temporal lobe in the twelve months following their stroke.References1. Manning EN, et al. e4 Is Associated with Disproportionate Progressive Hippocampal Atrophy in AD. PLoS ONE2014;9(5):e97608.2. Brodtmann A, et al. Charting cognitive and volumetric trajectories after stroke: Protocol for the Cognition And Neocortical Volume After Stroke (CANVAS) study. Int J Stroke2014;9(6):824–828.

scholarly journals APOE ε4 allele modified the correlation between deep grey matter volume and cognitive performance in non-demented elders

2020 ◽  
Vol 3 (3) ◽  
pp. 152-161
Author(s):  
Weiping Li ◽  
Yu Xie ◽  
Tingting Yu ◽  
Wenbo Wu ◽  
Kun Wang ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Grey Matter ◽  
Early Stage ◽  
Apoe Genotype ◽  
Grey Matter Volume ◽  
Matter Volume ◽  
Apoe Ε4 ◽  
Deep Grey Matter ◽  
Ε4 Allele ◽  
The Right

Abstract APOE ε4 allele is the strongest predictor of Alzheimer’s disease (AD) risk, but its role in the association between the deep grey matter volume and cognitive impairment is still unclear. This study investigated the effects of APOE ε4 allele on this association in non-demented elders. We enrolled 24 patients with mild cognitive impairment (MCI) and 28 normal controls (NC), who underwent the whole brain 3DTIW MRI scanning, an APOE genotype test, and neuropsychological tests. The right thalamus (p = 0.026), the left pallidum (p = 0.026), and the bilateral amygdala (left p = 0.042, right p = 0.048) atrophied in MCI, and their volume were positively correlated with the cognitive scores (MoCA) (p < 0.05). Furthermore, the general liner regression model suggested that the correlation between the right thalamus and the putamen volume with MoCA scores was different in the APOE ε4 carriers and non- carriers. Compared with the non APOEε4 carriers, the right thalamus atrophied more rapidly when the cognition decline in APOE ε4 carriers, while the right putamen compensatory expansion to slow the rate of cognitive decline although failed. This suggested that the right putamen showed stronger compensation by increasing the volume at the early stage of cognitive impairments in the APOE ε4 carriers, while this compensatory change had been disappeared in the right thalamus. In conclusion, APOE ε4 allele modifies the correlation between the right thalamus, the right putamen, and MoCA scores, and it has a potential selective effect on the relationship between cognition and brain structures to some extent in non-demented elders.

Dementia, asymmetry of temporal lobe structures, and Apolipoprotein E genotype: Relationships to cerebral atrophy and neuropsychological impairment

2002 ◽  
Vol 8 (7) ◽  
pp. 925-933 ◽  
Author(s):  
ERIN D. BIGLER ◽  
DAVID F. TATE ◽  
MICHAEL J. MILLER ◽  
SARA A. RICE ◽  
CORY D. HESSEL ◽  
...  
Keyword(s):  
Temporal Lobe ◽  
Apoe Genotype ◽  
Cerebral Atrophy ◽  
Hippocampal Volume ◽  
Neuropsychological Performance ◽  
Intracranial Volume ◽  
Risk Effect ◽  
Ε4 Allele ◽  
The Right ◽  
Apoe Genotypes

We examined asymmetry of hippocampal volume as well as other temporal lobe structures (temporal lobe, temporal horn of the lateral ventricular system, parahippocampal and fusiform gyri) in 194 subjects from the Cache County, Utah study, with varying disorders [85 with Alzheimer's disease (AD), 59 with some cognitive or neuropsychiatric disorder—referenced as a Mixed Neuropsychiatric group, 30 with mild ambiguous/mild cognitive impairment (MA/MCI) and 20 controls] and APOE genotypes. Asymmetry was determined by subtracting left-side volume from the right corrected by total intracranial volume. No significant asymmetry was observed to be associated with presence of the ε4 allele. Since the AD-ε4 allele risk effect may be expressed early in the course of the disorder, we also examined asymmetry indices in AD, MA/MCI and Mixed Neuropsychiatric subjects early in the course of their disorder (2 years or less) to those with longer duration illness (greater than 2 years). We observed a leftward asymmetry (i.e., left side larger) regardless of APOE genotype in hippocampal volume where both AD and MCI subjects demonstrated a leftward shift in hippocampal size when length of disease (LOD) was less but not more than 2 years. Leftward asymmetry was not associated with LOD in the Mixed Neuropsychiatric group. These findings do not support an association between ε4 and hippocampal asymmetry in dementia. We also examined whether asymmetry influenced neuropsychological performance, but minimal effects were observed. Where significance or strong trends were observed, better neuropsychological performance was associated with larger parenchymal volume of temporal lobe structures. These findings were interpreted as representing cognitive reserve effects where larger volume was protective against impairment. The role of asymmetry research in understanding neuropsychological performance in dementia is discussed. (JINS, 2002, 8, 925–933.)

scholarly journals Free-water metrics in medial temporal lobe white matter tract projections relate to longitudinal cognitive decline

2020 ◽  
Author(s):  
Derek B. Archer ◽  
Elizabeth E. Moore ◽  
Niranjana Shashikumar ◽  
Logan Dumitrescu ◽  
Kimberly R. Pechman ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Executive Function ◽  
White Matter ◽  
Cognitive Decline ◽  
Temporal Lobe ◽  
Medial Temporal Lobe ◽  
Hippocampal Volume ◽  
White Matter Tract ◽  
Uncinate Fasciculus ◽  
Inferior Longitudinal Fasciculus

AbstractObjectiveHippocampal volume is a sensitive marker of neurodegeneration and a well-established predictor of age-related cognitive impairment. Recently, free-water (FW) magnetic resonance imaging (MRI) has shown associations with pathology in Alzheimer’s disease (AD), but it is still unclear whether these metrics are associated with measures of cognitive impairment. Here, we investigate whether FW and FW-corrected fractional anisotropy (FAT) within medial temporal lobe white matter tracts (cingulum, fornix, uncinate fasciculus, inferior longitudinal fasciculus, and tapetum) provides meaningful contribution to cognition and cognitive decline beyond hippocampal volume.Participants and MethodsVanderbilt Memory & Aging Project participants (n=319, 73±7 years, 59% male) with normal cognition and mild cognitive impairment (40% of cohort) underwent baseline brain MRI, including structural MRI to quantify hippocampal volume, diffusion MRI to quantify medial temporal lobe white matter tract FW and FAT, and longitudinal neuropsychological assessment with a mean follow-up of 3.5 years. Linear regressions were conducted to determine how hippocampal volume and white matter tract FW and FAT interact with baseline memory and executive function performances. Competitive model analyses determined the unique variance provided by white matter tract FW and FAT beyond that of hippocampal volume and other comorbidities. Linear mixed-effects models were conducted to determine how baseline hippocampal volume and white matter tract FW and FAT interact to explain longitudinal change in memory and executive function performances.ResultsFW in the inferior longitudinal fasciculus, tapetum, uncinate fasciculus, and cingulum were robustly associated with baseline memory and executive function. Further, competitive model analysis showed that tract FW contributed unique variance beyond other comorbidities and hippocampal volume for memory (ΔRadj2 range: 0.82-2.00%) and executive function (ΔRadj2 range: 0.88-1.87%). Longitudinal analyses demonstrated significant interactions of hippocampal volume and FAT in the inferior longitudinal fasciculus (p=0.02), tapetum (p=0.02), uncinate fasciculus (p=0.02), and cingulum (p=0.002) with decline in memory. For decline in executive function, we found significant interactions of hippocampal volume and FAT in inferior longitudinal fasciculus (p=0.03), tapetum (p=0.02), uncinate fasciculus (p=0.02), and fornix (p=0.02), as well as cingulum (p=0.02) and fornix (p=0.02) FW.ConclusionsOur results highlight novel associations between FW and FAT measures of medial temporal lobe tract microstructure and cognitive performance such that individuals with smaller hippocampal volumes and lower tract microstructure experience greater cognitive decline. These results suggest that white matter has a unique role in cognitive decline and, therefore, could be used to provide better disease staging, allowing for more precise disease monitoring in AD.

Discriminating accuracy of medial temporal lobe volumetry and fMRI in mild cognitive impairment

Hippocampus ◽  
2009 ◽  
Vol 19 (2) ◽  
pp. 166-175 ◽  
Author(s):  
Anne M. Jauhiainen ◽  
Maija Pihlajamäki ◽  
Susanna Tervo ◽  
Eini Niskanen ◽  
Heikki Tanila ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Temporal Lobe ◽  
Medial Temporal Lobe

Medial temporal lobe atrophy, but not CSF biomarkers, correlates with cognitive impairment in Alzheimer's disease

2021 ◽  
Vol 429 ◽  
pp. 119059
Author(s):  
Edoardo Barvas ◽  
Chiara Monaldini ◽  
Roberto Frusciante ◽  
Mirco Volpini ◽  
Beatrice Viti ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Temporal Lobe ◽  
Medial Temporal Lobe ◽  
Csf Biomarkers ◽  
Medial Temporal Lobe Atrophy ◽  
Lobe Atrophy

scholarly journals Increased functional connectivity within medial temporal lobe in mild cognitive impairment

Hippocampus ◽  
2012 ◽  
Vol 23 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Sandhitsu R. Das ◽  
John Pluta ◽  
Lauren Mancuso ◽  
Dasha Kliot ◽  
Sylvia Orozco ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Functional Connectivity ◽  
Temporal Lobe ◽  
Medial Temporal Lobe

scholarly journals Atrophy and cognitive profiles in older adults with temporal lobe epilepsy are similar to mild cognitive impairment

Brain ◽  
2020 ◽  
Author(s):  
Erik Kaestner ◽  
Anny Reyes ◽  
Austin Chen ◽  
Jun Rao ◽  
Anna Christina Macari ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Older Adults ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Medial Temporal Lobe ◽  
Late Onset ◽  
Amnestic Mild Cognitive Impairment

Abstract Epilepsy incidence and prevalence peaks in older adults yet systematic studies of brain ageing and cognition in older adults with epilepsy remain limited. Here, we characterize patterns of cortical atrophy and cognitive impairment in 73 older adults with temporal lobe epilepsy (&gt;55 years) and compare these patterns to those observed in 70 healthy controls and 79 patients with amnestic mild cognitive impairment, the prodromal stage of Alzheimer’s disease. Patients with temporal lobe epilepsy were recruited from four tertiary epilepsy surgical centres; amnestic mild cognitive impairment and control subjects were obtained from the Alzheimer’s Disease Neuroimaging Initiative database. Whole brain and region of interest analyses were conducted between patient groups and controls, as well as between temporal lobe epilepsy patients with early-onset (age of onset &lt;50 years) and late-onset (&gt;50 years) seizures. Older adults with temporal lobe epilepsy demonstrated a similar pattern and magnitude of medial temporal lobe atrophy to amnestic mild cognitive impairment. Region of interest analyses revealed pronounced medial temporal lobe thinning in both patient groups in bilateral entorhinal, temporal pole, and fusiform regions (all P &lt; 0.05). Patients with temporal lobe epilepsy demonstrated thinner left entorhinal cortex compared to amnestic mild cognitive impairment (P = 0.02). Patients with late-onset temporal lobe epilepsy had a more consistent pattern of cortical thinning than patients with early-onset epilepsy, demonstrating decreased cortical thickness extending into the bilateral fusiform (both P &lt; 0.01). Both temporal lobe epilepsy and amnestic mild cognitive impairment groups showed significant memory and language impairment relative to healthy control subjects. However, despite similar performances in language and memory encoding, patients with amnestic mild cognitive impairment demonstrated poorer delayed memory performances relative to both early and late-onset temporal lobe epilepsy. Medial temporal lobe atrophy and cognitive impairment overlap between older adults with temporal lobe epilepsy and amnestic mild cognitive impairment highlights the risks of growing old with epilepsy. Concerns regarding accelerated ageing and Alzheimer’s disease co-morbidity in older adults with temporal lobe epilepsy suggests an urgent need for translational research aimed at identifying common mechanisms and/or targeting symptoms shared across a broad neurological disease spectrum.

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