Hippocampal shape across the healthy lifespan and its relationship with cognition

Bussy, Aurélie; Plitman, Eric; Tullo, Stephanie; Salaciak, Alyssa; Bedford, Saashi A.; Farzin, Sarah; Béland, Marie-Lise; Valiquette, Vanessa; Kazazian, Christina; Tardif, Christine; Devenyi, Gabriel A.; Chakravarty, M. Mallar

doi:10.1016/j.neurobiolaging.2021.03.018

Cited by 28 publications

(19 citation statements)

References 127 publications

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“…Interestingly, MTL subregions are also affected in typical aging, and dissociating normal from early pathological changes is sometimes challenging (Fjell et al, 2014). For example, studies report a decline in HPC and ERC volumes with age (Schuff et al, 1999;Jernigan et al, 2001;Du et al, 2006), and trajectories appear to differ across MTL subregions with linear vs. non-linear atrophy over the whole lifespan (Ziegler et al, 2012;Fjell et al, 2013;de Flores et al, 2015;Daugherty et al, 2016;Hasan et al, 2016;Bussy et al, 2021). Thus, a better understanding of the effects of age on the MTL subregions is essential to define the best candidate to be used as an AD biomarker.…”

Section: Introductionmentioning

confidence: 99%

Medial Temporal Lobe Subregional Atrophy in Aging and Alzheimer's Disease: A Longitudinal Study

Chauveau

Kuhn

Palix

et al. 2021

Front. Aging Neurosci.

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Medial temporal lobe (MTL) atrophy is a key feature of Alzheimer's disease (AD), however, it also occurs in typical aging. To enhance the clinical utility of this biomarker, we need to better understand the differential effects of age and AD by encompassing the full AD-continuum from cognitively unimpaired (CU) to dementia, including all MTL subregions with up-to-date approaches and using longitudinal designs to assess atrophy more sensitively. Age-related trajectories were estimated using the best-fitted polynomials in 209 CU adults (aged 19–85). Changes related to AD were investigated among amyloid-negative (Aβ−) (n = 46) and amyloid-positive (Aβ+) (n = 14) CU, Aβ+ patients with mild cognitive impairment (MCI) (n = 33) and AD (n = 31). Nineteen MCI-to-AD converters were also compared with 34 non-converters. Relationships with cognitive functioning were evaluated in 63 Aβ+ MCI and AD patients. All participants were followed up to 47 months. MTL subregions, namely, the anterior and posterior hippocampus (aHPC/pHPC), entorhinal cortex (ERC), Brodmann areas (BA) 35 and 36 [as perirhinal cortex (PRC) substructures], and parahippocampal cortex (PHC), were segmented from a T1-weighted MRI using a new longitudinal pipeline (LASHiS). Statistical analyses were performed using mixed models. Adult lifespan models highlighted both linear (PRC, BA35, BA36, PHC) and nonlinear (HPC, aHPC, pHPC, ERC) trajectories. Group comparisons showed reduced baseline volumes and steeper volume declines over time for most of the MTL subregions in Aβ+ MCI and AD patients compared to Aβ− CU, but no differences between Aβ− and Aβ+ CU or between Aβ+ MCI and AD patients (except in ERC). Over time, MCI-to-AD converters exhibited a greater volume decline than non-converters in HPC, aHPC, and pHPC. Most of the MTL subregions were related to episodic memory performances but not to executive functioning or speed processing. Overall, these results emphasize the benefits of studying MTL subregions to distinguish age-related changes from AD. Interestingly, MTL subregions are unequally vulnerable to aging, and those displaying non-linear age-trajectories, while not damaged in preclinical AD (Aβ+ CU), were particularly affected from the prodromal stage (Aβ+ MCI). This volume decline in hippocampal substructures might also provide information regarding the conversion from MCI to AD-dementia. All together, these findings provide new insights into MTL alterations, which are crucial for AD-biomarkers definition.

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Section: Introductionmentioning

confidence: 99%

Medial Temporal Lobe Subregional Atrophy in Aging and Alzheimer's Disease: A Longitudinal Study

Chauveau

Kuhn

Palix

et al. 2021

Front. Aging Neurosci.

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“…The hippocampus is located in the deep layer of the brain tissue and belongs to the limbic system. It is the center of information processing, is closely related to memory, learning and other cognitive functions and focuses on regulating spatial memory and short-term memory [12] . Therefore, the hippocampus was used as the target brain region for this study and the mechanism of Alzheimer's-like neurodegenerative disease in mice was investigated by establishing a ketamine abuse model.…”

Section: Resultsmentioning

confidence: 99%

Ketamine Promotes Alzheimer’s-Like Neurodegeneration by Activating Glycogen Synthase Kinase 3 Beta and Inhibiting Protein Phosphatase 2A

Fan¹

2022

IJPS

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Fan: Ketamine Promoting Alzheimer-Like Neurodegeneration in MiceTo investigate the mechanism of ketamine promoting Alzheimer's-like neurodegeneration in mice. 24 male 8 w old Kunming mice of specific pathogen-free grade were randomly divided into a blank control group (control group) and a ketamine intervention group (experimental group) according to the random number table, 12 mice in each group. The mice in the experimental group were given ketamine injection at the dose of 30 mg/kg. Mice in the control group were given an equal volume of normal saline injection. The intervention was conducted once a day for consecutive 6 mo. The behavioral changes of the mice in the two groups were compared. Western blot was used to detect the expression levels of tau (phospho Thr231), tau (phospho S396), tau (phospho Ser404), glycogen synthase kinase 3 beta, glycogen synthase kinase 3 beta (phospho ser9) and protein phosphatase 2A proteins in the brain tissue of hippocampus and the ratio of phosphorylated tau protein to tau protein was calculated. The expressions of beta-amyloid protein and tau protein in the hippocampus were observed by immunohistochemistry. The results of the Morris water maze showed that the escape latency of mice in both groups was gradually decreased and the escape latency of mice in the control group was lower than that in the experimental group. Besides, the times of crossing target platform and the proportion of activity time in target quadrant of mice in the experimental group were lower than those in the control group. At the same time, compared with the control group, the expression levels of tau (phospho Thr231) and tau (phospho Ser404) were decreased in the experimental group, and the expressions of tau (phospho S396), glycogen synthase kinase 3 beta, glycogen synthase kinase 3 beta (phospho ser9) and protein phosphatase 2A proteins were increased. Compared with the control group, the expression of beta-amyloid protein in the experimental group was significantly reduced and the opalescence density of beta-amyloid protein was significantly lower than that in the control group (p<0.05). Long-term use of ketamine can lead to up-regulated expression of beta-amyloid protein and tau protein in mice hippocampus, which may induce hyperphosphorylation of tau protein at Thr231, S396 and S404 by activating glycogen synthase kinase 3 beta and inhibiting protein phosphatase 2A, causing cognitive function decline in mice.

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“…Verbal fluency is a cognitive ability with relative stability during aging, especially in women [ 61 ], and declines in memory can be observed from midlife, with accelerated deterioration after 60 years; this is associated with lower hippocampal volume, and lower education [ 62 , 63 ] increases the probability of future dementia and neurodegenerative disorders on postmenopausal women [ 64 ].…”

Section: Discussionmentioning

confidence: 99%

Pilates and Cognitive Stimulation in Dual Task an Intervention Protocol to Improve Functional Abilities and Minimize the Rate of Age-Related Cognitive Decline in Postmenopausal Women

Silva

Torres

Ericeira

et al. 2022

IJERPH

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It is already known the effectiveness of Pilates training on cognitive and functional abilities. It is also known that dual-task exercise and cognitive stimuli improve cognition and functional capacity. However, no previous report combined cognitive stimuli and Pilates in dual task and measured its effects on the cognitive and physical performances of postmenopausal women. Objective: To apply an interventional dual-task (PILATES-COG) protocol and to evaluate its influence on memory, language, and functional physical performances on healthy, community-dwelling postmenopausal older women. Methods: 47 women with amenorrhea for at least 12 months participated in this study. Those allocated on the PILATES-COG group underwent a 12-week, twice a week regimen of 50 min sessions of simultaneous mat Pilates exercise program and cognitive tasks. Cognitive and physical functional performance were assessed. Two-way mixed ANOVA was used for data analysis, and Bonferroni post hoc tests were used for within- and between-group comparisons. Results: The PILATES-COG group showed significant improvement after the intervention in semantic verbal fluency (p < 0.001; ηρ² = 0.268), phonological verbal fluency (p < 0.019; ηρ² = 0.143), immediate memory (p < 0.001; ηρ² = 0.258), evocation memory (p < 0.001 ηρ² = 0.282), lower-limb muscle strength (p < 0.001; ηρ² = 0.447), balance (p < 0.001; ηρ² = 0.398), and dual-ask cost (p < 0.05; ηρ² = 0.111) assessments on healthy, community-dwelling postmenopausal older women. Conclusion: This is the first report of a feasible and effective approach using Pilates and cognitive stimulation in dual task for the reduction of age-related cognitive decline and the improvement of physical functional performance in healthy postmenopausal women.

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Hippocampal shape across the healthy lifespan and its relationship with cognition

Cited by 28 publications

References 127 publications

Medial Temporal Lobe Subregional Atrophy in Aging and Alzheimer's Disease: A Longitudinal Study

Medial Temporal Lobe Subregional Atrophy in Aging and Alzheimer's Disease: A Longitudinal Study

Ketamine Promotes Alzheimer’s-Like Neurodegeneration by Activating Glycogen Synthase Kinase 3 Beta and Inhibiting Protein Phosphatase 2A

Pilates and Cognitive Stimulation in Dual Task an Intervention Protocol to Improve Functional Abilities and Minimize the Rate of Age-Related Cognitive Decline in Postmenopausal Women

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