| Autor: |
Ortiz GG; Department of Philosophical and Methodological Disciplines, University Health Sciences Center, University of Guadalajara, Guadalajara 44340, Jalisco, Mexico.; Postgraduate Gerontology Program, University Health Sciences Center, University of Guadalajara, Guadalajara 44340, Jalisco, Mexico., Ramírez-Jirano J; Neurosciences Division, Western Biomedical Research Center, Mexican Social Security Institute, IMSS, Guadalajara 44340, Jalisco, Mexico., Arizaga RL; Public Health Department, School of Medicine, University of Buenos Aires, Buenos Aires C1121ABG, Argentina., Delgado-Lara DLC; Department of Philosophical and Methodological Disciplines, University Health Sciences Center, University of Guadalajara, Guadalajara 44340, Jalisco, Mexico.; Departamento Académico de Formación Universitaria, Ciencias de la Salud, Universidad Autónoma de Guadalajara, Zapopan 45129, Jalisco, Mexico., Torres-Sánchez ED; Department of Medical and Life Sciences, University Center of la Cienega, University of Guadalajara, Ocotlan 47820, Jalisco, Mexico. |
| Abstrakt: |
Frontotemporal lobar degeneration (FTLD) belongs to a heterogeneous group of highly complex neurodegenerative diseases and represents the second cause of presenile dementia in individuals under 65. Frontotemporal-TDP is a subgroup of frontotemporal dementia characterized by the aggregation of abnormal protein deposits, predominantly transactive response DNA-binding protein 43 (TDP-43), in the frontal and temporal brain regions. These deposits lead to progressive degeneration of neurons resulting in cognitive and behavioral impairments. Limbic age-related encephalopathy (LATE) pertains to age-related cognitive decline primarily affecting the limbic system, which is crucial for memory, emotions, and learning. However, distinct, emerging research suggests a potential overlap in pathogenic processes, with some cases of limbic encephalopathy displaying TDP-43 pathology. Genetic factors play a pivotal role in both disorders. Mutations in various genes, such as progranulin (GRN) and chromosome 9 open reading frame 72 (C9orf72), have been identified as causative in frontotemporal-TDP. Similarly, specific genetic variants have been associated with an increased risk of developing LATE. Understanding these genetic links provides crucial insights into disease mechanisms and the potential for targeted therapies. |
