ALS/FTD: Evolution, Aging, and Cellular Metabolic Exhaustion.
aging
amyotrophic lateral sclerosis
evolution
metabolism
motor neuron disease
protein
Journal
Frontiers in neurology
ISSN: 1664-2295
Titre abrégé: Front Neurol
Pays: Switzerland
ID NLM: 101546899
Informations de publication
Date de publication:
2022
2022
Historique:
received:
05
03
2022
accepted:
19
04
2022
entrez:
17
6
2022
pubmed:
18
6
2022
medline:
18
6
2022
Statut:
epublish
Résumé
Amyotrophic lateral sclerosis and frontotemporal dementia (ALS/FTD) are neurodegenerations with evolutionary underpinnings, expansive clinical presentations, and multiple genetic risk factors involving a complex network of pathways. This perspective considers the complex cellular pathology of aging motoneuronal and frontal/prefrontal cortical networks in the context of evolutionary, clinical, and biochemical features of the disease. We emphasize the importance of evolution in the development of the higher cortical function, within the influence of increasing lifespan. Particularly, the role of aging on the metabolic competence of delicately optimized neurons, age-related increased proteostatic costs, and specific genetic risk factors that gradually reduce the energy available for neuronal function leading to neuronal failure and disease.
Identifiants
pubmed: 35711269
doi: 10.3389/fneur.2022.890203
pmc: PMC9196861
doi:
Types de publication
Journal Article
Langues
eng
Pagination
890203Informations de copyright
Copyright © 2022 Henderson, Kepp and Eisen.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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