Molecular Hydrogen Neuroprotection in Post-Ischemic Neurodegeneration in the Form of Alzheimer's Disease Proteinopathy: Underlying Mechanisms and Potential for Clinical Implementation-Fantasy or Reality?

Int J Mol Sci. 2022 Jun 13;23(12):6591. doi: 10.3390/ijms23126591.

Abstract

Currently, there is a lot of public interest in naturally occurring substances with medicinal properties that are minimally toxic, readily available and have an impact on health. Over the past decade, molecular hydrogen has gained the attention of both preclinical and clinical researchers. The death of pyramidal neurons in especially the CA1 area of the hippocampus, increased permeability of the blood-brain barrier, neuroinflammation, amyloid accumulation, tau protein dysfunction, brain atrophy, cognitive deficits and dementia are considered an integral part of the phenomena occurring during brain neurodegeneration after ischemia. This review focuses on assessing the current state of knowledge about the neuroprotective effects of molecular hydrogen following ischemic brain injury. Recent studies in animal models of focal or global cerebral ischemia and cerebral ischemia in humans suggest that hydrogen has pleiotropic neuroprotective properties. One potential mechanism explaining some of the general health benefits of using hydrogen is that it may prevent aging-related changes in cellular proteins such as amyloid and tau protein. We also present evidence that, following ischemia, hydrogen improves cognitive and neurological deficits and prevents or delays the onset of neurodegenerative changes in the brain. The available evidence suggests that molecular hydrogen has neuroprotective properties and may be a new therapeutic agent in the treatment of neurodegenerative diseases such as neurodegeneration following cerebral ischemia with progressive dementia. We also present the experimental and clinical evidence for the efficacy and safety of hydrogen use after cerebral ischemia. The therapeutic benefits of gas therapy open up new promising directions in breaking the translational barrier in the treatment of ischemic stroke.

Keywords: amyloid; brain ischemia; dementia; molecular hydrogen; neurodegeneration; neuroprotection; tau protein.

Publication types

  • Review

MeSH terms

  • Alzheimer Disease* / drug therapy
  • Amyloid
  • Amyloidogenic Proteins
  • Animals
  • Brain Ischemia* / drug therapy
  • Brain Ischemia* / metabolism
  • Fantasy
  • Hydrogen / pharmacology
  • Hydrogen / therapeutic use
  • Ischemia
  • Neuroprotection
  • tau Proteins / metabolism

Substances

  • Amyloid
  • Amyloidogenic Proteins
  • tau Proteins
  • Hydrogen

Grants and funding

This research received no external funding.