ArticleNeuroinformatics2026
A Perovskite Memdiode-Based Neuromorphic in Silico Surrogate Model for Emulating Predictive Coding Failure in Diabetic Neuropathy.
Article in Neuroinformatics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Halide perovskite memdiodes have coupled ionic-electronic dynamics and are promising candidates for artificial synapses in neuromorphic computing. We provide an in silico neuromorphic circuit that includes a comprehensive perovskite memdiode model and confirm its synaptic plasticity repertoire through simulation-based validation. The proposed model recapitulates analog long-term potentiation/depression (LTP/LTD), spike-timing-dependent plasticity (STDP), spike-rate-dependent plasticity (SRDP), and paired-pulse facilitation/depression (PPF/PPD). We also describe pulse-amplitude- and pulse-width-dependent conductance modulation, pinched hysteresis I-V curves, and statistical robustness to device-to-device and cycle-to-cycle fluctuations through Monte Carlo simulation. This memdiode is implemented into a continuous-time neuromorphic predictive coding framework to minimize Variational Free Energy (VFE). In this architecture, we directly map four clinical hallmarks of diabetic peripheral neuropathy (DPN)-plasticity impairment, homeostatic failure, afferent attenuation, and conduction delay-to localized circuit parameters ([Formula: see text]). One severity parameter α is used to continuously tune the network between healthy predictive coding and computational collapse. Healthy baseline parameters minimize VFE quickly. Moderate DPN (α = 0.5) results in permanently elevated oscillatory VFE, a hypothetical counterpart of allodynia. Severe DPN (α ≥ 0.8) paralyzes the homeostatic plasticity, and the system collapses to a frozen maladaptive state that is similar to sensory ataxia. The noise resilience analysis and hyperparameter sensitivity analysis indicate that the architecture is highly resilient to stochasticity within the simulated parameter space and structurally robust to hyperparameter perturbations in all dynamical regimes. The primary contribution of this work is a computational framework demonstrating how second-order, BCM-capable memristive device dynamics can be used to model systems-level predictive-coding failure; the behaviorally validated perovskite memdiode model and the DPN severity mapping serve as a concrete, illustrative instantiation of this framework.
Indexed as
Identifiers
42627467What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.