The hypothalamus is an early site of mitochondrial failure and neuro-immune circuit disruption in amyotrophic lateral sclerosis
Ontology highlight
ABSTRACT:
INSTRUMENT(S):
ORGANISM(S): Mus Musculus (mouse)
TISSUE(S): Brain
SUBMITTER: 
Viviana Greco
LAB HEAD: Viviana Greco
PROVIDER: PXD070931 | Pride | 2026-04-06
REPOSITORIES: Pride
Dataset's files
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| SODG93A_Hyp2_run1.raw | Raw | |||
| SODG93A_Hyp2_run2.raw | Raw | |||
| SODG93A_Hyp2_run3.raw | Raw | |||
| SODG93A_Hyp3_run1.raw | Raw | |||
| SODG93A_Hyp3_run2.raw | Raw |
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Publications
The hypothalamus is an early site of mitochondrial failure and neuro-immune circuit disruption in amyotrophic lateral sclerosis.
Scaricamazza Silvia S Nesci Valentina V Fenili Gianmarco G Tiberi Marta M Percio Anna A Rosina Marco M Salvatori Illari I Riggio Flaminia F Candelise Niccolò N Pieroni Luisa L Greco Viviana V Chiurchiù Valerio V Ferri Alberto A Valle Cristiana C
Molecular metabolism 20260401
<h4>Background</h4>Metabolic dysfunction is a defining feature of amyotrophic lateral sclerosis (ALS), emerging early and strongly associated with disease progression and prognosis. While systemic hypermetabolism is well documented, the central mechanisms underlying energy imbalance remain poorly understood. The hypothalamus, a key regulator of whole-body energy homeostasis, has recently been implicated in ALS, but its mechanistic contribution to metabolic failure and disease progression remains ...[more]
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