Purpose: One possible cause for surgical failure following temporal lobectomy for the treatment of epilepsy due to classical hippocampal sclerosis (CHS) is the presence of more widespread cortical changes. Neocortical changes in CHS shown by quantitative neuroimaging studies may involve hippocampal projection pathways. Our aim was to quantitate neocortical pathology using a postmortem series of brains from patients with epilepsy and CHS.
Methods: Sections from 13 cortical regions from both left and right hemispheres, including hippocampal projection pathways, were examined from nine epilepsy patients with unilateral CHS (4), bilateral CHS (2), non-CHS (3), and non-epilepsy controls (4). Using GFAP, CD68, and NPY immunohistochemistry as markers of acquired neocortical pathology, quantitative analysis of the staining fractions in the cortex and white matter was carried out.
Key Findings: Higher staining fractions were observed for all markers in both cortex and white matter in CHS patients, which was significantly different for CD68 and NPY compared to controls (p < 0.05) but not to non-CHS epilepsy cases. There was no significant difference between staining fractions in left and right hemispheres for unilateral CHS cases. Regional analysis showed preferential gliosis and microgliosis of temporal poles, frontal poles, and orbitofrontal cortex in epilepsy cases.
Significance: This study supports acquired neocortical pathology in epilepsy patients both with and without CHS. Cortical pathology does not show lateralization to the side of CHS. Preferential involvement of the temporal and frontal poles may relate to other factors, such as cortical injury associated with seizures, rather than involvement through hippocampal pathways.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1111/j.1528-1167.2010.02773.x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Abnormal cytoskeletal remodeling but normal neuronal excitability in a mouse model of the recurrent developmental and epileptic encephalopathy-susceptibility KCNB1-p.R312H variant.
Commun Biol
December 2024
Department of Neuroscience and Cell Biology, Robert Wood Johnson Medical School, Rutgers University, Piscataway, NJ, USA.
Integrin_K Channel_Complexes (IKCs), are implicated in neurodevelopment and cause developmental and epileptic encephalopathy (DEE) through mechanisms that were poorly understood. Here, we investigate the function of neocortical IKCs formed by voltage-gated potassium (Kv) channels Kcnb1 and α5β5 integrin dimers in wild-type (WT) and homozygous knock-in (KI) Kcnb1 mouse model of DEE. Kcnb1 mice suffer from severe cognitive deficit and compulsive behavior.
View Article and Find Full Text PDFCognitive decline profiles associated with lewy pathology in the context of Alzheimer's disease neuropathologic change.
Alzheimers Res Ther
December 2024
Shiley-Marcos Alzheimer's Disease Research Center, Department of Neurosciences, University of California, San Diego, CA, USA.
Background: Alzheimer's disease neuropathologic change (ADNC) and Lewy pathology (LP) often coexist in cognitively impaired individuals. These pathologies' relative distribution and severity may modify these individuals' clinical presentation, cognitive profile, and prognosis. Therefore, we examined the contributions of LP and concomitant ADNC to disease survival and profiles of cognitive decline in preclinical and clinical stages in a large neuropathologically diagnosed group.
View Article and Find Full Text PDFConnectivity, Pathology, and ApoE4 Interactions Predict Longitudinal Tau Spatial Progression and Memory.
Hum Brain Mapp
December 2024
Department of Neuroscience, UC Berkeley, Berkeley, California, USA.
Tau pathology spread into neocortex indicates a transition from healthy aging to Alzheimer's disease (AD). Connectivity between tau epicenters and later accumulating regions of cortex has been proposed as a mechanism of tau spread, but how this relationship changes with greater AD pathology burden or genotype is not understood. We investigated tau accumulation in two key regions, precuneus and inferior temporal cortex, using resting state functional connectivity (rsFC) and longitudinal PET imaging from a multicohort sample of cognitively unimpaired older adults.
View Article and Find Full Text PDFLocus coeruleus tau is linked to successive cortical tau accumulation.
Alzheimers Dement
December 2024
Institute of Human Behavioral Medicine, Medical Research Center, Seoul National University, Seoul, Seoul, Republic of Korea.
Article Synopsis
- The study explored the correlation between tau accumulation in the locus coeruleus (LC) and its relationship with tau levels in various cortical regions based on Braak stages, particularly focusing on the influence of amyloid beta (Aβ) deposition.
- A total of 170 participants underwent advanced imaging techniques, including tau and amyloid PET scans, revealing a significant relationship between LC tau burden and global tau accumulation, especially in individuals with Aβ positivity.
- While LC tau did not directly affect memory, it was linked to delayed memory through various pathways, highlighting LC tau as a potential indicator for cognitive decline in Alzheimer's disease.
A novel monomeric amyloid β-activated signaling pathway regulates brain development via inhibition of microglia.
Elife
December 2024
Departments of Neurology and Neuroscience, University of Wisconsin-Madison, Madison, United States.
Amyloid β (Aβ) forms aggregates in the Alzheimer's disease brain and is well known for its pathological roles. Recent studies show that it also regulates neuronal physiology in the healthy brain. Whether Aβ also regulates glial physiology in the normal brain, however, has remained unclear.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!