Molecular and Cellular Research of Neuroprotection and Neurodegeneration

Dear Colleagues,

Neurodegenerative diseases are marked by the gradual loss of specific neuron populations. While the exact initial cause of neuronal death remains unknown, aging is widely regarded as a significant risk factor. Many of these diseases are associated with abnormal accumulations of misfolded peptides or proteins in the brain and spinal cord. Over time, these insoluble peptide or protein deposits may build up and become more toxic in older neurons. The accumulation of neurodegeneration-related proteins, including Aβ1–42 peptide, hyperphosphorylated Tau, and α-synuclein, disrupts neuronal and glial intracellular pathways. This altered signaling impacts protein quality control, mitochondrial function, autophagy, and lysosomal processes, and can lead to the formation of stress granules, synaptic toxicity, neuroinflammation, and an impaired innate immune response.

At the level of signal transduction, where cellular pathways dictate whether neurons survive or die, neuroprotective signaling pathways such as JAK/STAT, Wnt/β-catenin, PI3K/Akt, MAPK/ERK, and Nrf2 are crucial. In a similar vein, neurotrophic substances like BDNF promote neuronal development and plasticity through TrkB receptors, which are essential in the fight against neurodegenerative stresses. Instead of providing protection, these pathways may become dysregulated and contribute to neurodegeneration. On the other hand, degenerative pathways that cause cell death and are linked to illnesses like Alzheimer's and Parkinson's disease include excessive calcium signaling, mitochondrial malfunction, and chronic inflammation.

Understanding how signaling pathways contribute to both neuroprotection and neurodegeneration offers valuable insights for therapeutic interventions aimed at enhancing neuronal resilience and slowing degenerative processes. By targeting key pathways within these intricate cellular networks, researchers can work toward developing innovative treatments that stabilize or halt neurodegeneration.

This Special Issue aims to present cutting-edge research exploring the molecular and cellular pathways involved in neuroprotection and neurodegeneration, with a particular emphasis on signal transduction mechanisms. Neurodegenerative disorders, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis, are marked by progressive neuronal loss and functional decline, posing significant health and societal challenges. The complex signaling cascades governing neuronal survival, plasticity, and cell death provide crucial insights into the mechanisms underlying neurodegeneration and open avenues for therapeutic intervention.

We invite contributions that investigate signal transduction pathways involved in, but not limited to, the following:

• Synaptic signaling and plasticity;
• Oxidative stress and mitochondrial dysfunction;
• Inflammatory responses in the central nervous system;
• Therapeutic targets for Alzheimer’s disease;
• Therapeutic targets for Parkinson’s disease;
• Apoptosis and autophagy regulation in neurons;
• Protein aggregation and degradation pathways;
• Neurotrophic signaling and growth factor responses;
• Calcium homeostasis and excitotoxicity;
• New insights regarding different signaling pathways that can be involved in neurodegenerative diseases.

Dr. Nidhi Puranik
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Neurology International is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

• neurotrophic signaling
• synaptic signaling
• apoptosis
• neuroprotective signaling pathways
• neurotrophic factor
• neurodegenerative disorders
• stress signaling
• targeted therapy for neurodegenerative disorders
• Alzheimer's disease, Parkinson's disease
• Huntington's disease
• amyotrophic lateral sclerosis
• calcium signaling
• mitochondrial malfunction