{"doi":"10.3389/fncel.2024.1385783","title":"Editorial: Reviews in cellular neurophysiology 2022: neurophysiological mechanisms in the aging brain","abstract":"advancing age [3]. Neuroinflammation, stemming from various mechanisms, emerges as a pivotal factor in numerous diseases, as well as age-related neurodegeneration more broadly. This mechanism could contribute to the development of age-related ailments such as Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and others [4].Unraveling the underlying mechanisms of general neuroinflammation and neurophysiological changes in the aging brain could hold the key for the identification and rational development of neuroprotective therapies that could prove to be beneficial in a multitude of age-related neurodegenerative diseases.One approach to assess neuroinflammation was reviewed by Karvandi et al. (Karvandi et al., 2023). The authors provide a broad perspective on shared mechanisms underlying neuronal loss in neurodegenerative diseases during aging. The authors explore the interconnected pathways leading to neuronal cell death, with a focus on endoplasmic reticulum (ER) stress, oxidative stress, and neuroinflammation. This overview sets the stage for understanding the aging-related intricacies of neuronal loss and suggests potential neuroprotective strategies. The authors note that mechanisms such as protein misfolding and aggregation, mitochondrial dysfunction, generation of reactive oxygen species (ROS), and activation of the innate immune response are the most critical hallmarks of common neurodegenerative diseases. Consequently, they review ER stress, oxidative stress, and neuroinflammation as major pathological factors of neuronal cell death and discuss the neuroprotective effects of approaches that target these pathways.In line with the observation that molecular stress can cause neurological diseases is a contribution describing the function of cyclin-dependent kinase 5 (Cdk5). As reviewed by Ao and colleagues (Ao et al., 2022), Cdk5 is critical for the development of the nervous system, the migration and differentiation of neurons, the formation of synapses, and axon regeneration. The authors comprehensively review the involvement of Cdk5 in several age-related neurological diseases such as AD, PD, ALS, multiple sclerosis (MS) and others. Their review sheds light on the role of Cdk5 during neuronal development and in the aging nervous system. Highlighting the role of Cdk5 in various neurological disorders and its potential as a therapeutic target, the article underscores the importance of understanding its associated physiological and pathological mechanisms in the aging brain. This exploration into Cdk5 offers valuable insights into agingrelated aberrations and potential avenues for targeted treatments. Finally, Ao's outlook of the potential therapeutic applicability of Cdk5 inhibitors seems promising, while the need for the development of more selective inhibitors is brought to attention.Fleming aligns seamlessly with the focus on stress-induced changes in neurophysiology, exploring the intricate role of ATP13A2 in various neurodegenerative conditions, including PD, Kufor-Rakeb Syndrome, neuronal ceroid lipofuscinosis, hereditary spastic paraplegia, and ALS (Croucher and Fleming, 2024). The article discusses how ATP13A2 mutations may interact with environmental exposures, emphasizing the relevance of gene-environment interactions in the brain, particularly the vulnerable basal ganglia. In line with this, the authors discuss that heavy metal toxicity including manganese, iron, and zinc has been connected to ATP13A2 dysfunction. By unraveling common pathological mechanisms, the review contributes to a deeper understanding of ATP13A2related disorders and their implications for impairment of cellular neurophysiology.Finally, the research article by Yu et al. (Yu et al., 2023) aims to understand the role of Piezo1, a mechanosensitive ion channel, in astrocytes of the mouse cerebellum. Through a battery of experiments involving electrophysiological recordings, calcium imaging, and cell migr","journal":"Frontiers in Cellular Neuroscience","year":2024,"id":494750,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":0,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.948,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2024-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":672831,"name":"Steven M. Graves","orcid":"0000-0003-2291-1617","position":1,"is_corresponding":false},{"id":1163616,"name":"Markus Rießland","orcid":"0000-0003-2592-5045","position":2,"is_corresponding":false},{"id":352649,"name":"Joshua L. Plotkin","orcid":"0000-0001-6232-7613","position":0,"is_corresponding":true}],"reference_count":4,"raw_metadata":null,"created_at":"2026-07-19T02:09:11.736910Z","pmid":"38486711","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}