Several lines of evidence can be used to try to answer the question of whether epilepsy is a progressive disease, and whether persistent seizures, or the underlying process itself, cause neuronal injury. The results of clinical studies have been inconclusive. Neuroimaging studies offer a quantitative approach. In patients with temporal lobe epilepsy, structural magnetic resonance imaging (MRI) has shown volume reductions ipsilateral to the epileptic focus in hippocampal and extrahippocampal regions; the former, in cross-sectional studies, increase with increasing epilepsy duration. Other factors associated with increasing hippocampal atrophy include a history of complex or prolonged febrile seizures, and generalized tonic-clonic seizure number. Positron emission tomography (PET) has shown supporting results. However, these studies have been cross-sectional rather than longitudinal. Preliminary results from prospective imaging studies using fluorodeoxyglucose PET and volumetric MRI show that patients with more recent seizure onset are less likely to have hypometabolism or volume loss than those with a long history of epilepsy. Alternate interpretations of these data include a possible progressive effect of epilepsy, or a tendency for patients with structural or functional findings at seizure onset to be more likely to develop uncontrolled epilepsy. In addition to the human studies that have been performed, parallel investigations in animal models using some of the same imaging techniques may help to unravel the factors associated with neuronal injury due to seizures, and aid in interpreting results of clinical studies.
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http://dx.doi.org/10.1016/S0079-6123(02)35028-3 | DOI Listing |
Mol Brain
January 2025
Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou, Jiangsu, 215006, China.
Commun Biol
January 2025
Mitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, TX, USA.
Aggregation of microtubule-associated tau protein is a distinct hallmark of several neurodegenerative disorders such as Alzheimer's disease (AD), dementia with Lewy bodies (DLB), and progressive supranuclear palsy (PSP). Tau oligomers are suggested to be the primary neurotoxic species that initiate aggregation and propagate prion-like structures. Furthermore, different diseases are shown to have distinct structural characteristics of aggregated tau, denoted as polymorphs.
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January 2025
State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, 518055, China.
Sterile alpha and Toll/interleukin-1 receptor motif containing 1 (SARM1), a nicotinamide adenine dinucleotide (NAD)-utilizing enzyme, mediates axon degeneration (AxD) in various neurodegenerative diseases. It is activated by nicotinamide mononucleotide (NMN) to produce a calcium messenger, cyclic ADP-ribose (cADPR). This activity is blocked by elevated NAD level.
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January 2025
NMPA Key Laboratory for Research and Evaluation of Narcotic and Psychotropic Drugs, Xuzhou, China.
Neuroinflammation is a key factor in the pathogenesis of Parkinson's disease (PD). Activated microglia in the central nervous system (CNS) and infiltration of peripheral immune cells contribute to dopaminergic neuron loss. However, the role of peripheral immune responses, particularly triggering receptor expressed on myeloid cells-1 (TREM-1), in PD remains unclear.
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January 2025
Department of Pharmacology and Chemical Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Microglia are progressively activated by inflammation and exhibit phagocytic dysfunction in the pathogenesis of neurodegenerative diseases. Lipid-droplet-accumulating microglia were identified in the aging mouse and human brain; however, little is known about the formation and role of lipid droplets in microglial neuroinflammation of Alzheimer's disease (AD). Here, we report a striking buildup of lipid droplets accumulation in microglia in the 3xTg mouse brain.
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