Preprint Review Version 1 This version is not peer-reviewed

Hypoxia Pathways in Parkinson’s Disease: From Pathogenesis to Therapeutic Targets

Version 1 : Received: 5 September 2024 / Approved: 6 September 2024 / Online: 6 September 2024 (13:00:58 CEST)

How to cite: Gao, Y.; Zhang, J.; Tang, T.; Liu, Z. Hypoxia Pathways in Parkinson’s Disease: From Pathogenesis to Therapeutic Targets. Preprints 2024, 2024090517. https://doi.org/10.20944/preprints202409.0517.v1 Gao, Y.; Zhang, J.; Tang, T.; Liu, Z. Hypoxia Pathways in Parkinson’s Disease: From Pathogenesis to Therapeutic Targets. Preprints 2024, 2024090517. https://doi.org/10.20944/preprints202409.0517.v1

Abstract

The human brain is highly dependent on oxygen, utilizing approximately 20% of the body’s oxygen at rest. Oxygen deprivation to the brain can lead to loss of consciousness within seconds and death within minutes. Recent studies have identified regions of the brain with spontaneous episodic hypoxia, referred to as "hypoxic pockets." Hypoxia can also result from impaired blood flow due to conditions such as heart disease, blood clots, stroke, or hemorrhage, as well as from reduced oxygen intake or excessive oxygen consumption caused by factors like low ambient oxygen, pulmonary diseases, infections, inflammation, and cancer. Severe hypoxia in the brain can manifest symptoms similar to Parkinson’s disease (PD), including cerebral edema, mood disturbances, and cognitive impairments. Additionally, the development of PD appears to be closely associated with hypoxia and hypoxic pathways. This review seeks to investigate the molecular interactions between hypoxia and PD, emphasizing the pathological role of hypoxic pathways in PD and exploring their potential as therapeutic targets.

Keywords

Parkinson’s disease; hypoxia; hypoxia pathways; neurodegenerative diseases; transmembrane protein 175; DJ-1; LRRK2

Subject

Biology and Life Sciences, Neuroscience and Neurology

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