ArticleJournal of neuropathology and experimental neurology2014
Hippocampal sclerosis in dementia, epilepsy, and ischemic injury: differential vulnerability of hippocampal subfields.
Article in Journal of neuropathology and experimental neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed.
- Characterizing the MRI signature of hippocampal sclerosis of aging.Alzheimer's research & therapy · 2026Article
- Development of cognitive, motor, metabolic, and mutant huntingtin aggregation in the zQ175 mouse model of Huntington's disease.Scientific reports · 2025Article
- TDP-43-proteinopathy at the crossroads of tauopathy: on copathology and current and prospective biomarkers.Frontiers in cellular neuroscience · 2025Review
- Limbic-predominant age-related TDP-43 encephalopathy (LATE-NC): Co-pathologies and genetic risk factors provide clues about pathogenesis.Journal of neuropathology and experimental neurology · 2024Review
- Brain Banking in Dementia Studies.Methods in molecular biology (Clifton, N.J.) · 2024Review
- A novel histological staging of hippocampal sclerosis that is evident in gray matter loss in vivo.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Article
- RGS14 limits seizure-induced mitochondrial oxidative stress and pathology in hippocampus.Neurobiology of disease · 2023Article
- Repetitive head impacts and chronic traumatic encephalopathy are associated with TDP-43 inclusions and hippocampal sclerosis.Acta neuropathologica · 2023Article
- RGS14 is neuroprotective against seizure-induced mitochondrial oxidative stress and pathology in hippocampus.bioRxiv : the preprint server for biology · 2023Article
- Impaired Behavioral Pattern Separation in Refractory Temporal Lobe Epilepsy and Mild Cognitive Impairment.Journal of the International Neuropsychological Society : JINS · 2022Article
- Limbic-Predominant Age-Related TDP-43 Encephalopathy: Medical and Pathologic Factors Associated With Comorbid Hippocampal Sclerosis.Neurology · 2022Article
- NADPH Oxidase: a Possible Therapeutic Target for Cognitive Impairment in Experimental Cerebral Malaria.Molecular neurobiology · 2022Article
- Hypoxia/Ischemia-Induced Rod Microglia Phenotype in CA1 Hippocampal Slices.International journal of molecular sciences · 2022Article
- Low Subicular Volume as an Indicator of Dementia-Risk Susceptibility in Old Age.Frontiers in aging neuroscience · 2022Article
- Asymmetry of Hippocampal Tau Pathology in Primary Age-Related Tauopathy and Alzheimer Disease.Journal of neuropathology and experimental neurology · 2021Article
- Early Selective Vulnerability of the CA2 Hippocampal Subfield in Primary Age-Related Tauopathy.Journal of neuropathology and experimental neurology · 2021Article
- Proteomic differences in the hippocampus and cortex of epilepsy brain tissue.Brain communications · 2021Article
- Limbic Predominant Age-Related TDP-43 Encephalopathy (LATE): Clinical and Neuropathological Associations.Journal of neuropathology and experimental neurology · 2020Article
- Differential Atrophy in the Hippocampal Subfield Volumes in Four Types of Mild Dementia.Frontiers in neuroscience · 2020Article
- Targeting age-related differences in brain and cognition with multimodal imaging and connectome topography profiling.Human brain mapping · 2019Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Severe neuronal loss in the hippocampus, that is, hippocampal sclerosis (HS), can be seen in 3 main clinical contexts: dementia (particularly frontotemporal lobar degeneration [FTLD]), temporal lobe epilepsy (TLE), and hippocampal ischemic injury (H-I). It has been suggested that shared pathogenetic mechanisms may underlie selective vulnerability of the hippocampal subfields such as the CA1 in these conditions. We determined the extent of neuronal loss in cases of HS-FTLD (n=14), HS-TLE (n=35), and H-I (n=20). Immunohistochemistry for zinc transporter 3 was used to help define the CA3/CA2 border in the routinely processed human autopsy tissue samples. The subiculum was involved in 57% of HS-FTLD, 10% of H-I, and 0% of HS-TLE cases (p<0.0001). The CA regions other than CA1 were involved in 57% of HS-TLE, 30% of H-I, and 0% of HS-FTLD cases (p=0.0003). The distal third of CA1 was involved in 79% of HS-FTLD, 35% of H-I, and 37% of HS-TLE cases (p=0.02). The distal third of CA1 was the only area involved in 29% of HS-FTLD, 3% of HS-TLE, and 0% of H-I cases (p=0.019). The proximal-middle CA1 was the only area affected in 50% of H-I, 29% of HS-TLE, and 0% of HS-FTLD cases (p=0.004). These findings support heterogeneity in the pathogenesis of HS.
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