Intranasal Delivery of Mitochondria-Targeted Neuroprotective Drugs: A New Approach for Treating Traumatic Brain Injury

Researchers led by Jignesh D. Pandya, have identified a promising method for delivering neuroprotective drugs directly to the brain for treating traumatic brain injury (TBI) through intranasal administration, bypassing the blood-brain barrier (BBB).

Intranasal Delivery of Mitochondria-Targeted Neuroprotective Drugs A New Approach for Treating Traumatic Brain Injury

This non-invasive approach enhances drug bioavailability, reduces the need for high doses, and minimizes adverse side effects.


Focusing on compounds targeted at mitochondria—key regulators of cell death and damage following TBI—the study reviews the advantages of intranasal delivery over traditional methods.

It highlights successful applications in animal models, such as reducing stroke damage and reversing Alzheimer’s symptoms, and outlines the screening of compounds based on pharmacological properties for intranasal use.

This innovative strategy could significantly impact the treatment of TBI, especially in military settings, by offering a rapid, effective, and field-applicable method to counteract the progression of TBI pathogenesis.

Image Description:

Schematic representation of key aspects of intranasal delivery of neuroprotection compounds to the brain. TBI is difficult to treat as most therapeutic agents (98%) cannot reach in the brain, mainly due to the selective permeability of the blood–brain barrier (BBB). The olfactory and trigeminal nerves can serve as direct nose-to-brain routes that bypass the BBB that can impede absorption of most CNS targeted compounds, resulting in higher bioavailability. In addition, compared to traditional routes, the nasal administration of drugs can direct the rapid CNS absorption to brain tissues, thereby circumventing the hepatic first-pass metabolism and gastric degradation and allowing fast onset of pharmacological action.

Article DOI.

Image Credits: Pandya, J.D., Musyaju, S., Modi, H.R. et al. J Transl Med22, 167 (2024). 

© World Mitochondria Society (WMS)

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