DeCure's autonomous Neuro AI scientist is researching a drug-repurposing hypothesis for diabetic polyneuropathy — screening already-approved drugs against its 23-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleDiabetic polyneuropathy maps to a 23-gene Open Targets module — the target space DeCure's AI scientist screens approved drugs against.
DeCure.ai methodSignature reversal (LINCS) plus network proximity (STRING) rank already-approved drugs likely to perturb this module — the same engine that produces DeCure.ai's repurposing hypotheses.
Repurposing thesisScreening approved medicines against this disease module, then publishing the evidence for the strongest candidate. Known pharmacology and human exposure data make the first question sharper — they do not establish safety or efficacy in a new indication.
Research record
01
ResearchComing soon
Candidate research + dossier — target rationale, drug-repurposing thesis and evidence pack.proof: Published dossier + on-chain hash
02
ValidationComing soon
In-vitro biological validation at a contract research org (CRO).proof: CRO contract + in-vitro report
03
Peer review & paperComing soon
Peer-reviewed paper published open-access (preprint + journal).proof: DOI + open-access link + on-chain hash
Current lead
No approved-drug candidate for diabetic polyneuropathy is corroborated in the literature DeepSearch retrieved. Some conditions are managed with non-pharmacological care — a device, surgery or physical therapy — rather than a medicine; that may be the case here, or the literature we found may simply be too sparse yet to support a drug-repurposing angle.
Molecular view
centromere protein E (CENPE) — CENPE is one of the genes genetically linked to this disease in Open Targets — shown as context, not as a drug target we're pursuing: no approved-drug candidate for this disease is yet corroborated in the literature we found.
Loading structure…
helix sheet anpdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 8HFH · 1.8 Å · ligand PHOSPHOAMINOPHOSPHONIC ACID-ADENYLATE ESTER (ANP). Experimental structure, not a prediction.
What the evidence adds up to
Diabetic polyneuropathy occurs in about 50% of patients with diabetes mellitus, and its prevalence in the general population is 1.66%, rising to 6.6% in people older than 60 years. In a population-based analysis of 2,892 cases and 14,435 matched controls, diabetic polyneuropathy was the most common specific subtype, accounting for 38.2% of all polyneuropathies. Diabetes with end-organ disease was present in 46.8% of cases versus 6.5% of controls. Cases had a higher median Charlson comorbidity index (6 versus 3) and a considerably higher median modified Rankin Scale score (4 versus 1). Polyneuropathy was an independent contributor to difficulty walking (odds ratio 1.9), climbing stairs (2.0), using an assistive device (2.0), fall tendency (2.4), work disability (4.2), lower limb amputations (3.9), and opioid use (2.7). Prevalent cases died at a younger median age than controls (80 versus 86 years), and incident cases had a six-month shorter survival.
Ideas about the pathogenesis have evolved to include direct insulin signalling on neurons, actions of cleaved C-peptide, abnormal signalling by advanced glycation endproducts, and activation of poly (ADP-ribose) polymerase in microvessels and neurons. Manipulation of these pathways may offer new therapeutic approaches, but a 2008 review noted that recent clinical trials addressing pathogenesis have been largely disappointing. A 2002 systematic overview stated that intensive glycaemic control remains the only effective specific therapy currently available. A 2025 review of pharmacological correction described treatment as built on relieving symptoms and eliminating pathophysiological links, but it provided no new trial data showing that any drug alters the course of the disease.
What is still missing are clinical trials that convincingly target the newly identified pathogenic mechanisms and show benefit beyond glycaemic control. The 2008 review called for a new round of pathogenesis-directed trials, but no such trial has yet produced a disease-modifying therapy. The population data show that diabetic polyneuropathy is underidentified in routine coding, which complicates patient stratification for trials. Funding for adequately powered, long-term studies that measure functional impairment and survival, rather than only pain scores, remains insufficient.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Current Opinion in Neurology · 2008 · 142 citations
Diabetic polyneuropathy: an update
AbstractPURPOSE OF REVIEW: To examine current issues in the diagnosis and treatment of diabetic polyneuropathy. RECENT FINDINGS: Diabetic neuropathies are common and rising in prevalence with the global burden of type 2 diabetes. Polyneuropathy is also emerging as a complication of impaired glucose tolerance, without frank diabetes. Ideas about the pathogenesis of diabetic polyneuropathy have evolved, and some new pathogenic mechanisms are being considered. These include roles for direct insulin signaling on neurons and axons that transduce growth signals, actions of the cleaved C-peptide product of the insulin prohormone, abnormal signaling by advanced glycation endproducts on neuronal and glial receptors and activation of poly (ADP-ribose) polymerase in microvessels and neurons. Manipulation of these pathways may offer new therapeutic approaches. Ideas about neuronal targets in the treatment of neuropathic pain have also advanced emphasizing abnormal sodium and calcium channel signaling. SUMMARY: Consideration of diabetic polyneuropathy as a unique neurodegenerative condition has generated interest in new pathways involved in its development. A new round of clinical trials that address its pathogenesis may be welcome, as recent attempts have been largely disappointing. In the interim, several forms of therapy for neuropathic pain are available.
Impairments and comorbidities of polyneuropathy revealed by population-based analyses
AbstractOBJECTIVE: To quantify polyneuropathy impairments and comorbidities utilizing the Rochester Epidemiology Project (2010 census = 148,201). METHODS: ICD-9-CM coding identified polyneuropathy cases (2006-2010) and their 5:1 age- and sex-matched controls. Mortality and impairments were evaluated while identifying and adjusting for Charlson Index comorbidities. RESULTS: Overall prevalence of polyneuropathy was 1.66%, and markedly rose to 6.6% in persons older than 60 years. Cases (n = 2,892) had more comorbidities than controls (n = 14,435) with higher median Charlson Index (6 vs 3, p < 0.001). Diabetes with end-organ disease represented the largest increased comorbidity in cases compared with controls (46.8% vs 6.5%). Diabetic polyneuropathy was the most common specific subtype (38.2%). Miscoded idiopathic cases and false-negative controls also commonly had diabetic polyneuropathy. Median modified Rankin Scale score was considerably higher for cases than controls (4 vs 1, p < 0.001). Multiple comorbidities were found associated with polyneuropathy after adjusting for diabetes co-occurrence, including pulmonary disease, dementia, and others. Polyneuropathy was an independent contributor to multiple functional impairments including difficulty walking (odds ratio [OR] = 1.9), climbing stairs (OR = 2.0), using an assistive device (OR = 2.0), fall tendency (OR = 2.4), work disability (OR = 4.2), lower limb amputations (OR = 3.9), and opioid use (OR = 2.7). Prevalent cases had a younger median age at death than controls (80 vs 86 years, p < 0.001), and incident cases had a 6-month shorter survival. CONCLUSIONS: Polyneuropathies have notable neurologic impairments beyond their identified multiple comorbidities. Life expectancy is shortened. Diabetic polyneuropathy is underidentified. The quantified extent of the disease burden and refined comorbidity associations emphasize that greater research efforts and health care initiatives are needed.
DOAJ (DOAJ: Directory of Open Access Journals) · 2015 · 3 citations
Diabetic polyneuropathy: from science to practice
AbstractDiabetes mellitus (DM) is one of the most common causes of polyneuropathy worldwide. In accordance with the modern classification, there are typical and atypical forms of generalized diabetic polyneuropathy (DPN) some of which have differing pathogenesis and clinical manifestations. The questions of pathogenesis and diagnostic principles for the most common form - typical DPN - are considered. The main approaches to the treatment of patients with DPN are discussed: 1) glycemic control, 2) lifestyle recommendations, 3) pathogenetic therapy, 4) symptomatic treatment. Pathogenetic therapy includes administration of alpha-lipoic acid (ALA). Berlithion® is an ALA widely used in neurological practice which proved to be effective and demonstrated high safety profile in the treatment of DPN.
Ural Medical Journal · 2025 · 0 citations · open access
Modern Methods of Pharmacological Correction of Diabetic Polyneuropathy
AbstractIntroduction . Typical diabetic sensorimotor polyneuropathy is one of the complications of diabetes mellitus, occurring in 50 % of patients with this pathology. Diabetic neuropathy as a complication of diabetes mellitus requires additional drug correction in order to improve the quality of life. The aim of the work is to study modern approaches and the effectiveness of pharmacological correction of diabetic polyneuropathy based on scientific literature data over the past 10 years. Materials and methods. Analysis and systematization of scientific publications posted in the PubMed, Scopus, Web of Science databases for 2014–2023. Results and discussion . The work presents the clinical characteristics of typical diabetic polyneuropathy. Particular emphasis is placed on pharmacological correction and consideration of most classes of drugs that can relieve pain. Treatment tactics are built not only on relieving the main symptoms, but also on eliminating the pathophysiological component of the disease. However, treatment is based not only on symptomatic therapy, but also on the elimination of pathogenetic links of this pathology. Conclusion . Diabetic polyneuropathy is a formidable complication in people suffering from diabetes mellitus. The main goal of treatment is to relieve pain and prevent the development of complications. Correction is provided by a wide range of pharmacological drugs.
Journal of the Peripheral Nervous System · 2002 · 0 citations
STATUS OF CURRENT CLINICAL TRIALS IN DIABETIC POLYNEUROPATHY
AbstractPeripheral polyneuropathy is the most frequent complication of diabetic mellitus. In spite of many clinical trials of different specific interventions for diabetic polyneuropathy, intensive glycemic control remains the only effective specific therapy currently available for this troublesome complication. This systematic overview reports the status of current clinical trials in diabetic polyneuropathy with an emphasis on those interventions directed towards specific pathophysiological derangements. A discussion of clinical trials of agents directed towards relieving painful symptoms of diabetic polyneuropathy concludes this overview.
Disease module: DeepOracle (Open Targets). Structures: RDKit from PubChem SMILES. Literature: retrieved by DeepSearch across 234,678,978 indexed works (targeted per-candidate search), resolved on OpenAlex.
DeCure is a research and publication project, not medical advice and not a treatment. "DeCure for X" describes a research goal, not a claim that a cure exists. Backing a cure is a contribution to fund the research — it is not an investment, and confers no yield, royalty, equity or IP ownership. Papers are published open-access by the DeCure.ai DAO.
