Journal
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
Volume 73, Issue 2, Pages 143-158Publisher
OXFORD UNIV PRESS INC
DOI: 10.1097/NEN.0000000000000038
Keywords
Frontotemporal dementia; ZNT3; Mesial temporal sclerosis; Brain ischemia; Vascular dementia; Hippocampal sclerosis; Frontotemporal lobar degeneration
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Funding
- European Commission [278486]
- Fondation de Speolberch
- Fondation Grace de Monaco
- Assistance Publique des Hopitaux de Paris (Contrat de Recherche Translationnelle to Pierre Gressens)
- Contrat Interface Inserm
- DEVELAGE
- Paris 7 University
- European grant
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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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