DeCure for Distal hereditary motor neuropathy type 2
DeCure's autonomous Neuro AI scientist is researching a drug-repurposing hypothesis for distal hereditary motor neuropathy type 2 — screening already-approved drugs against its 6-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleDistal hereditary motor neuropathy type 2 maps to a 6-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 distal hereditary motor neuropathy type 2 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
heat shock protein family B (small) member 8 (HSPB8) — HSPB8 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 apo structuredrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 8S7A · 1.951 Å · ligand none (apo structure). Experimental structure, not a prediction.
What the evidence adds up to
The 1991 study of arsenic neuropathy in 13 patients found marked sensory nerve conduction abnormalities alongside moderate motor nerve conduction changes, with motor studies and EMG typical of axonal degeneration confirmed by sural nerve biopsy. This is not hereditary motor neuropathy but toxic axonal injury, and no drug was tested.
A 1992 study detected hereditary motor sensory neuropathy type I (HMSN I) in 17 of 36 children under 10 who had an affected parent. Four children had slowed motor nerve conduction velocities by age one or younger. Clinical signs were subtle: pes planus, distal foot wasting, weak ankle eversion and dorsiflexion, and areflexia. No treatment or drug was investigated.
A 2023 case report of a 29-year-old man with hereditary sensory and autonomic neuropathy type II describes complications since childhood. The authors state that lack of early diagnosis led to an unfavourable prognosis and poor life condition despite efforts to maintain quality of life. No drug is mentioned, and no intervention altered the course.
No abstract addresses distal hereditary motor neuropathy type 2 specifically. No drug, no trial, no survival or response rate data exist in these abstracts for that disease. What is missing is any funded clinical trial for distal hereditary motor neuropathy type 2, any validated patient stratification, and any drug candidate tested in a controlled setting.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Journal of Neurology Neurosurgery & Psychiatry · 1991 · 44 citations · open access
Electrophysiological profile in arsenic neuropathy.
AbstractComprehensive electrophysiological studies were performed on 13 patients with arsenic neuropathy. The most prominent finding was a marked abnormality in sensory nerve conduction in the presence of moderate abnormalities in motor nerve conduction. The motor nerve conduction studies and needle EMG were typical of those seen in axonal degeneration which was confirmed by sural nerve biopsy.
Journal of Neurology Neurosurgery & Psychiatry · 1992 · 15 citations · open access
Detection of hereditary motor sensory neuropathy type I in childhood.
AbstractClinical signs and slowed motor nerve conduction velocities were found in 17 of 36 children under 10 years of age who had one parent with hereditary motor sensory neuropathy type I (HMSN I). Four children had slowed conduction velocities at one year or less. Clinical signs were subtle and included pes planus, distal foot wasting, weakness of ankle eversion and dorsiflexion and areflexia. HMSN I can be detected reliably in children, even before one year of age.
Clinical Case Reports · 2023 · 3 citations · open access
A rare case of hereditary sensory and autonomic neuropathy type II
AbstractWe describe the follow-up of a 29-year-old man diagnosed with hereditary sensory and autonomic neuropathy type II, including the different complications that presented since his childhood. Despite efforts to maintain an optimal quality of life, the lack of an early diagnosis led to an unfavorable prognosis and life condition.
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.
