{"doi":"10.1111/jns.12681","title":"A call to action for peripheral neuropathy research funding—Time to consolidate funding under one <scp>NIH</scp> initiative?","abstract":"Peripheral neuropathies (PNs) pose a significant clinical challenge in the field of neurological disorders, with a prevalence of 2.4% in the general population that rises with age to over 8% in patients aged 55 years and older.1 Symmetrical, distal-to-proximal axonal loss is the most common form of PN and accounts for most cases.2, 3 It is characterized by damage to the peripheral nerves that typically, especially for diabetes (the leading cause of PN), impacts small-diameter axons beginning in the feet and progresses proximally in a length-dependent manner. PN results in a range of debilitating symptoms such as numbness, tingling, weakness, as well as burning or shooting pain.4 Along with these painful symptoms, patients may experience depression, anxiety, and sleep disturbances.5 As PN progresses, individuals may present with diminished sensation to mechanical and thermal stimuli, making it challenging to perceive or effectively heal injuries or trauma, which increases the risk of non-healing ulcers. In severe cases, the cumulative effects of sensation loss and non-healing ulcers can necessitate lower limb amputations.6 In fact, patients with PN are almost four times at greater risk of undergoing lower-limb amputation than those without.7 Additionally, PN also leads to an increased risk of falls due to compromised balance and proprioception, further exacerbating the potential for injury and disability in affected individuals. PN likely impacts far more tissues and organs than previously appreciated.8 Data now indicate diabetic PN exists in the muscle, liver, adipose tissue, pancreas, gastrointestinal tract, and heart.9-17 PN profoundly impacts the lives of patients, with limited therapeutic options to mitigate pain symptoms, prevent progression, or regenerate lost axons. While clinical presentations may appear similar, PN can result from a range of causes, including both inherited and acquired conditions. Hereditary neuropathies (HN), such as Charcot–Marie-Tooth (CMT) disease and hereditary sensory and autonomic neuropathies, comprise a diverse group of inherited PN disorders, with an overall prevalence of 1:2500.18 These differ in their inheritance patterns (autosomal dominant, recessive, or X-linked), electrophysiological characteristics (demyelinating, axonal, or intermediate), and clinical features. While not as common as the other PN types, HN highlight the importance of genetic factors in neuropathic disorders. Of the acquired neuropathies, diabetic peripheral neuropathy (DPN) is the most prevalent, accounting for 32%–53% of total cases.2 As cases of diabetes are expected to rise from 537 to 783 million by 2045, DPN, which affects 50% or more of patients and increases in frequency with disease duration, will also increase.19 Importantly, the Global Burden of Disease Study 2021 ranked DPN among the top 10 leading causes of ill health and disability worldwide.20 Chemotherapy-induced neuropathy (CIPN) is a challenging side effect of chemotherapeutic agents, affecting roughly half of patients undergoing cancer treatments,21 and may lead to dose reduction or premature cessation of chemotherapy, thus impeding treatment efficacy and worsening clinical outcomes.22 Additionally, neuropathic symptoms may persist in about one-third of cancer survivors after treatment cessation, severely affecting the quality of life.22 Inflammatory neuropathies, such as those observed in autoimmune conditions like Guillain-Barré syndrome, arise when the immune system directly attacks and damages nerve fibers, causing axonal degeneration, demyelination, and subsequent motor and sensory impairments.23 Infectious neuropathies, on the other hand, can result from direct infection or inflammatory responses triggered by pathogens such as human immunodeficiency virus, leprosy, or COVID-19. These infections can lead to nerve damage through mechanisms like viral replication within peripheral nerves, immune-mediated attacks, or the production of neurotoxic ","journal":"Journal of the Peripheral Nervous System","year":2025,"id":551151,"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":1,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9656,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2025-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":467169,"name":"Kristy L. Townsend","orcid":"0000-0002-2849-9195","position":1,"is_corresponding":false},{"id":1446599,"name":"Vincenza Spallone","orcid":"0000-0002-8905-216X","position":2,"is_corresponding":false},{"id":630419,"name":"Daniela M. Menichella","orcid":"0000-0002-2955-175X","position":3,"is_corresponding":false},{"id":973009,"name":"Emily J. Koubek","orcid":"0000-0001-6952-3326","position":4,"is_corresponding":false},{"id":255269,"name":"Eva L. Feldman","orcid":"0000-0002-9162-2694","position":5,"is_corresponding":false},{"id":350440,"name":"Stéphanie Eid","orcid":"0000-0003-3775-7544","position":0,"is_corresponding":true}],"reference_count":36,"raw_metadata":null,"created_at":"2026-07-19T02:54:20.915388Z","pmid":"39801027","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":[]}