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DOI 10.1016/j.niox.2024.11.006

Медицинская библиотека · Nitric oxide : biology and chemistry · 2024

Critical role of hydrogen sulfide in the management of neurodegenerative disease.

Pawar Rajashree, Pandey Dheeraj, Naqvi Saba, Sharma Abha

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Аннотация

Hydrogen sulfide has been known to humans for about 300 years and the previous studies emphasize only on its toxic side effects. In the last two decennium, researchers have varied their perspectives and insights towards H2S biology based on experimental findings. It has been found that H2S is an endogenic gaseous signaling molecule in many organisms and plays a crucial role in many systems and diseases. Early reports suggest that H2S as a neuromodulator influences calcium levels within the brain cells which ultimately control memory, learning, and cognition. It has also been observed that some complications in the pathogenesis of neurodegenerative diseases are due to anomalies in the biosynthesis and metabolism of H2S. This review focuses on the role of H2S in the pathophysiology of major neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, Huntington's disease and Vascular dementia. H2S was observed to have a protective role in the above-mentioned neurological conditions and the H2S donor therapy may help in disease management. The H2S gas displays a neuroprotective role and protects against cellular damage thereby declining the neurological conditions. Some studies have revealed that treatment with H2S donors has improved neuronal damage, restored memory and cognition in animal models. In this review, we have discussed the role of H2S donors as neuroprotective agents with examples of some of the natural and synthetic H2S donors, and also briefly enumerated the molecules used to detect H2S in neurodegenerative diseases.

Для цитирования: Pawar Rajashree, Pandey Dheeraj, Naqvi Saba, Sharma Abha. Critical role of hydrogen sulfide in the management of neurodegenerative disease.. Nitric oxide : biology and chemistry. 2024. DOI: 10.1016/j.niox.2024.11.006.

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