mTOR Signaling in Inflammation, Brain Injuries and Neurodegeneration

Dear Colleagues,

Neurodegeneration is characterized by overlapping impairment in processes including protein synthesis and degradation, protein misfolding and aggregation, activation of neuron cell death mechanisms, inflammation, gliosis, mitochondrial dysfunction, plasticity, and endo/exocytosis.

Neuroinflammation is characterized by the activation of innate immune response due to misfolded/aggregated proteins or systemic infections that trigger microglial and astroglial activation and the consequent release of inflammatory cytokines and chemokines. This response is intended to be beneficial at early stages, promoting aggregates and neuron debris clearance, but if inflammation becomes chronic, it exacerbates neurodegeneration.

These processes are modulated by signaling pathways that, regardless of the underlying core pathophysiological cause, are similarly impaired and associated with converging phenotypes including depression (in early stages of the diseases), motor symptoms, autonomic dysfunction, and dementia.

One of the key kinases involved in neurodegeneration and inflammation is the mechanistic target of rapamycin (mTOR).

This special issue of the International Journal of Molecular Sciences is dedicated to research papers and review articles regarding the involvement of mTOR/Akt signalling in neurodegeneration and the intertwined inflammatory processes that are triggered. We would like to cover mTOR-mediated mechanisms that contribute to synaptic dysfunction, neuron death, circuit impairment, micro- and astrogliosis and neuroinflammation and neurodegeneration.

We encourage authors to submit mTOR-related molecular studies in but not limited to:

1. a) a neurodegenerative context (AD, PD, HD, ALS).
2. b) stroke or traumatic brain injuries.
3. c) pathogenic infections affecting the brain, such as SARS-CoV-2 or HIV.

Prof. Dr. Cristina Malagelada
Guest Editor

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