Neuroprotective Mechanisms in Neurological Disorders

Neuroprotective mechanisms encompass a diverse array of endogenous processes and therapeutic strategies aimed at preserving neuronal structure and function in the face of acute injury or chronic degeneration. Central themes include the regulation of excitotoxicity through modulation of glutamatergic signalling, attenuation of oxidative stress via activation of antioxidant pathways such as Nrf2, and suppression of neuroinflammation by balancing pro- and anti-inflammatory cytokine networks. Maintenance of mitochondrial integrity, enhancement of autophagic clearance of protein aggregates and the stabilisation of metal ion homeostasis further contribute to neuronal survival. Endogenous peptides and growth factors engage intracellular cascades—most notably PI3K–Akt and ERK–MAPK—to promote cell survival and neurite outgrowth, while exogenous small molecules, peptidomimetics and nanomaterials offer routes to augment these pathways or to deliver cargo across the blood–brain barrier. Glial cells also play a critical role, both in providing trophic support through astrocyte-derived factors and in executing phagocytic clearance by microglia. Collectively, these mechanisms underpin an integrated defence that targets the molecular hallmarks of neurological disorders—amyloid and tau aggregation, dopaminergic loss, axonal injury and synaptic dysfunction—and inform the design of disease-modifying interventions with global health relevance.

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Neuroprotective Mechanisms in Neurological Disorders publication trend

The graph below shows the total number of articles in neuroprotective mechanisms in neurological disorders across all publications each year (not limited to Nature Index journals).

Technical terms

Amyloid-β (Aβ): Peptides derived from amyloid precursor protein that can aggregate into plaques and trigger neurotoxicity in Alzheimer’s disease.

Neuroprotective peptide: Small endogenous or synthetic peptides that engage survival pathways to shield neurons from excitotoxic, oxidative or inflammatory damage.

Oxidative stress: An imbalance between production of reactive oxygen species and antioxidant defences, leading to cellular damage.

PI3K–Akt pathway: A key intracellular signalling cascade that promotes cell survival, metabolism and growth in response to trophic factors.

Apoptosis: Programmed cell death involving caspase activation and DNA fragmentation, distinct from necrosis.

References

1. Exploring structural determinants of neuroprotection bias on novel glypromate conjugates with bioactive amines. European Journal of Medicinal Chemistry (2024).
2. Reduction in Hippocampal Amyloid-β Peptide (Aβ) Content during Glycine-Proline-Glutamate (Gly-Pro-Glu) Co-Administration Is Associated with Changes in Inflammation and Insulin-like Growth Factor (IGF)-I Signaling. International Journal of Molecular Sciences (2024).
3. Ameliorative Effects by Hexagonal Boron Nitride Nanoparticles against Beta Amyloid Induced Neurotoxicity. Nanomaterials (2022).