Multi-target action of β-alanine protects cerebellar tissue from ischemic damage.
Olga KopachDmitri A RusakovSergiy SylantyevPublished in: Cell death & disease (2022)
Brain ischemic stroke is among the leading causes of death and long-term disability. New treatments that alleviate brain cell damage until blood supply is restored are urgently required. The emerging focus of anti-stroke strategies has been on blood-brain-barrier permeable drugs that exhibit multiple sites of action. Here, we combine single-cell electrophysiology with live-cell imaging to find that β-Alanine (β-Ala) protects key physiological functions of brain cells that are exposed to acute stroke-mimicking conditions in ex vivo brain preparations. β-Ala exerts its neuroprotective action through several distinct pharmacological mechanisms, none of which alone could reproduce the neuroprotective effect. Since β-Ala crosses the blood-brain barrier and is part of a normal human diet, we suggest that it has a strong potential for acute stroke treatment and facilitation of recovery.
Keyphrases
- cerebral ischemia
- blood brain barrier
- single cell
- subarachnoid hemorrhage
- resting state
- white matter
- brain injury
- oxidative stress
- functional connectivity
- atrial fibrillation
- endothelial cells
- induced apoptosis
- rna seq
- physical activity
- high resolution
- cell death
- weight loss
- mass spectrometry
- mesenchymal stem cells
- endoplasmic reticulum stress
- drug induced