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Treating SCA1 Mice with Water-Soluble Compounds to Non-Specifically Boost Mitochondrial Function

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Cisplatin-induced mitochondrial dysfunction is associated with impaired cognitive function in rats.

Naomi Lomeli¹, Kaijun Di², Jennifer Czerniawski³

¹Department of Pathology & Laboratory Medicine, University of California Irvine, Irvine, CA, USA.

Free Radical Biology & Medicine

|December 3, 2016

Summary

Chemotherapy can cause cognitive impairment, but N-acetylcysteine may help. This study found cisplatin damages brain cells and impairs memory, while N-acetylcysteine shows protective effects against these chemotherapy side effects.

Keywords:

Chemotherapy Chemotherapy-related cognitive impairment (CRCI)Cisplatin (CDDP)DNA damage Hippocampal neurons Mitochondria N-acetylcysteine (NAC)Neural stem/precursor cells (NSCs)Oxidative stress

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Area of Science:

Neuroscience
Pharmacology
Oncology

Background:

Chemotherapy-related cognitive impairment (CRCI) presents significant neurological challenges with no current effective treatments.
Cisplatin, a common chemotherapeutic agent, is known to induce CRCI, necessitating research into its underlying mechanisms and potential mitigation strategies.

Purpose of the Study:

To investigate the mechanisms of cisplatin-induced hippocampal damage in a rat model and in vitro neuronal cultures.
To evaluate the neuroprotective potential of N-acetylcysteine against cisplatin-induced neurotoxicity and cognitive deficits.

Main Methods:

Chronic cisplatin administration in rats, alongside N-acetylcysteine treatment, followed by cognitive behavioral testing.
In vitro analysis of cisplatin-treated hippocampal neurons and neural stem cells (NSCs) assessing mitochondrial function, oxidative stress, and apoptosis.
Evaluation of dendritic branching and spine density in neuronal cultures.

Main Results:

Cisplatin induced significant cognitive impairments in rats across multiple memory tasks.
In vitro, cisplatin triggered mitochondrial dysfunction, increased oxidative stress, activated caspase-9, and reduced dendritic spine density.
N-acetylcysteine treatment mitigated oxidative stress, apoptosis, and dendritic spine loss, partially reversing cognitive deficits.

Conclusions:

Mitochondrial dysfunction and oxidative stress are key mechanisms underlying cisplatin-induced cognitive impairments.
N-acetylcysteine demonstrates therapeutic potential in ameliorating the neurotoxic effects of cisplatin, offering a promising avenue for CRCI management.