Topic: mitochondrial dysfunction

Mechanisms Underlying the Persistence of Cancer-Related Fatigue

Cancer-related fatigue is a prominent and debilitating side effect of cancer and its treatment. It can develop prior to diagnosis, generally peaks during cancer treatment, and can persist long after treatment completion. Its mechanisms are multifactorial, and its expression is highly variable. Unfortunately, treatment options are limited. Our research uses syngeneic murine models of cancer and cisplatin-based chemotherapy to better understand these mechanisms. Our data indicate that both peripherally and centrally processes may contribute to the developmental of fatigue. These processes include metabolic alterations, mitochondrial dysfunction, pre-cachexia, and inflammation. However, our data has revealed that behavioral fatigue can persist even after the toxicity associated with cancer and its treatment recover. For example, running during cancer treatment attenuates kidney toxicity while also delaying recovery from fatigue-like behavior. Additionally, administration of anesthetics known to disrupt memory consolidation at the time treatment can promote recovery, and treatment-related cues can re-instate fatigue after recovery. Cancer-related fatigue can also promote habitual behavioral patterns, as observed using a devaluation task. We interpret this data to suggest that limit metabolic resources during cancer promote the utilization of habit-based behavioral strategies that serve to maintain fatigue behavior into survivorship. This line of work is exciting as it points us toward novel interventional targets for the treatment of persistent cancer-related fatigue.

Redox and mitochondrial dysregulation in epilepsy

Epileptic seizures render the brain uniquely dependent on energy producing pathways. Studies in our laboratory have been focused on the role of redox processes and mitochondria in the context of abnormal neuronal excitability associated with epilepsy. We have shown that that status epilepticus (SE) alters mitochondrial and cellular redox status, energetics and function and conversely, that reactive oxygen species and resultant dysfunction can lead to chronic epilepsy. Oxidative stress and neuroinflammatory pathways have considerable crosstalk and targeting redox processes has recently been shown to control neuroinflammation and excitability. Understanding the role of metabolic and redox processes can enable the development of novel therapeutics to control epilepsy and/or its comorbidities.

INFLAMMATION‑LINKED MITOCHONDRIAL DYSFUNCTION IN PTSD SUSCEPTIBILITY

FENS Forum 2026

Alterations in WWOX protein and gene lead to mitochondrial dysfunction in amyotrophic lateral sclerosis

Gestational stress induces mitochondrial dysfunction in prefrontal cortex and depressive-like behavior in postpartum rats

Mir-34 family is involved in Chronic Social Defeat-induced vulnerability to mood disorders and cardiac mitochondrial dysfunctions

Mitochondrial dysfunction and depression : the chicken or the egg ?

Mitochondrial dysfunction in Rett syndrome mice models: studying a neurological disorder from synaptic metabolism perspective to find new treatment options

Naringenin modulates paraquat-induced oxidative stress and mitochondrial dysfunction in a cellular model of Parkinson’s disease (SH-SY5Y cells)

Sirtuins Modulators Counteract Mitochondrial Dysfunction In Chemical And Neonatal Hypoxia: Implication To Neurodevelopmental Disorders

Treatment with the CB1R antagonist rimonabant rescues brain mitochondrial dysfunction via inhibition of intra-mitochondrial protein kinase A signalling in a mouse model of Rett syndrome