Focus on Neuro-
Disease Modeling
Disease modeling with in vitro cellular systems allows researchers to recreate and study mechanisms of neurological disorders in controlled experimental settings. As patient-derived and genetically engineered neuronal models become more human-relevant and more complex, the challenge shifts to establishing robust, reproducible functional phenotypes that can be compared across studies.
In 2026, this focus brings together the newest Disease Modeling material we publish. You’ll find a broad range of content, spanning from expert webinars to additional supporting materials added as they become available. The emphasis is on electrophysiology and readouts from network to subcellular scale, plus practical strategies and shared best practices from the field.
Featured Content
Explore how human neural models are advancing research in brain development and neurological disease, from neuronal subtype programming to axonal vulnerability.
Presented by Nature Custom Media, this webcast brings together expert perspectives on building more informative in vitro models for studying disease mechanisms and neuronal function.
Explore by Disease Area
Parkinson's Disease (PD)
Parkinson’s disease is a progressive neurodegenerative disorder classically defined by the selective loss of dopaminergic neurons, dopamine depletion, and the accumulation of misfolded α-synuclein.
Beyond neuronal loss, PD is increasingly understood as a disorder of neuronal activity and circuit dynamics, with early changes in firing behavior, network coordination, and connectivity.
Relevant Metrics
Dysregulated neuronal excitability
- Mean Firing Rate (Hz)
- Spike Amplitude (μV)
Disrupted firing regularity
- Inter-Spike Interval (ISI) coefficient of variation (ISI-CV)
- ISI (ms) Distribution (Histogram)
Altered network synchronization
- Burst Frequency (Hz)
- Spikes within Bursts (%)
- Spikes per Burst
- Burst Peak Firing Rate (Hz)
Changes in network temporal organization
- Burst Duration (s)
- Inter-Burst Interval (IBI) coefficient of variation (IBI-CV)
- IBI (s) Distribution (Histogram)
Impaired signal propagation
- Neuron Conduction Velocity (m/s)
- Longest Latency (ms)
Disrupted axonal integrity
- Number of Analyzed Neurons with Branches
- Total Axon Length (μm)
Webinars
Blogs
Beyond Neurodegeneration: Functional Signatures of Parkinson’s Disease with HD-MEAs
Parkinson’s disease involves early dysfunction in neuronal activity and circuit dynamics, not only neuronal loss. This blog shows how HD-MEAs and MaxLab Live assays quantify functional metrics across single cells, networks, and axonal pathways in human-relevant PD models.
Publications
Modeling interregional propagation of α-synuclein in human striatal–midbrain assembloids
Electrophysiological Phenotype Characterization of Human iPSC‐Derived Neuronal Cell Lines by Means of High‐Density Microelectrode Arrays
Generation of Human Striatal-Midbrain Assembloids From Human Pluripotent Stem Cells to Model Alpha-Synuclein Propagation
A human striatal-midbrain assembloid model of alpha-synuclein propagation
DeePhys: A machine learning–assisted platform for electrophysiological phenotyping of human neuronal networks
Conferences
Amyotrophic Lateral Sclerosis and Frontotemporal Dementia
Amyotrophic lateral sclerosis and frontotemporal dementia are clinically distinct but biologically connected neurodegenerative disorders that can share genetic causes and overlapping molecular mechanisms.
Both diseases involve progressive neuronal dysfunction, altered excitability, synaptic and axonal changes, and network-level impairment that can be studied in human-relevant in vitro models.
Webinars
Resources
iPSC FTD Disease Poster
High-Density Microelectrode Arrays for Modeling, Phenotyping, and Screening in a Human Model of Frontotemporal Dementia
MxW - FCDI Application Note
Longitudinal Functional Profiling of HumaniPSC-derived Frontotemporal Dementia Neuronson HD-MEAs
Blogs
New Therapeutic Target in the Fight Against ALS
A Nature study presents a human iPSC-derived neuronal network model that reveals how TDP-43 dysfunction drives neurotoxicity in ALS/FTLD and highlights NPTX2 as a promising therapeutic target. Using MaxWell Biosystems' MaxOne HD-MEAs, the team captured high-resolution functional readouts of these networks, supporting detailed characterization from network down to single-cell features.
Publications
Axonal Eif5a hypusination controls local translation and mitigates defects in FUS-ALS
A model of human neural networks reveals NPTX2 pathology in ALS and FTLD
Conferences
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Pain
Chronic pain arises from persistent changes in sensory signaling pathways, where peripheral and central neurons can become abnormally excitable or sensitized.
Disease-relevant models can help investigate altered nociceptive signaling, spontaneous activity, and treatment responses in human neuronal systems.
User Voices
Modeling Pain-Related Nociceptive Networks with HD-MEA and Microfluidics
Publications
Development of an innervated human skin equivalent to model nociceptive circuitry in vitro
Analgesic effect of Botulinum toxin in neuropathic pain is sodium channel independent
Development of a Hypersensitivity Evaluation Method for Cultured Sensory Neurons Using Electrical Activity Recording
Epilepsy
Epilepsy is characterized by recurrent, abnormal electrical activity in the brain, often linked to excessive neuronal excitability and disrupted network synchronization.
In vitro seizure models can help study burst dynamics, recurrent activity, and network instability as functional features of hyperexcitable neural circuits.
Webinars
Publications
Elevated FKBP5 expression associates with epilepsy-related molecular changes and promotes neuronal hyperexcitability
Microscale maps of bursting dynamics across human hippocampal slices from epilepsy patients
Human iPSC-derived glutamatergic neurons with pathogenic KCNQ2 variants display hyperactive bursting phenotypes
The fast-dissociating D2 antagonist antipsychotic JNJ-37822681 is a neuronal Kv7 channel opener: Potential repurposing for epilepsy treatment
Kv7.2 loss-of-function causes early hyperexcitability and network remodelling
Multimodal evaluation of network activity and optogenetic interventions in human hippocampal slices
Closed-loop neurostimulation via expression of magnetogenetics-sensitive protein in inhibitory neurons leads to reduction of seizure activity in a rat model of epilepsy
- Neuropsychiatric Disorders
Neuropsychiatric disorders involve complex changes in brain development, synaptic function, circuit connectivity, and neural network activity.
Human neural models can help investigate subtle functional phenotypes that may not be captured by molecular or structural readouts alone.
User Voices
Modeling Neurodevelopmental Disorders with Human iPSC Networks on HD-MEA
Publications
Defective ventral neurogenesis due to midfetal Chd8 mutation drives autistic-like behavior in mice
Human iPSC-derived glutamatergic neurons with pathogenic KCNQ2 variants display hyperactive bursting phenotypes
Regulation of Dendrite and Dendritic Spine Formation by TCF20
Autism genes converge on asynchronous development of shared neuron classes
16p11.2 deletion is associated with hyperactivation of human iPSC-derived dopaminergic neuron networks and is rescued by RHOA inhibition in vitro
Loss of schizophrenia risk gene XPO7 disrupts neuronal excitability and network regularity via altered Na+ channel dynamics in human neurons
Recapitulation of Perturbed Striatal Gene Expression Dynamics of Donor’s Brains With Ventral Forebrain Organoids Derived From the Same Individuals With Schizophrenia
An orexin-sensitive subpopulation of layer 6 neurons regulates cortical excitability and anxiety behaviour
Other Diseases
Neurological and neurodegenerative diseases can affect different cell types, circuits, and disease mechanisms, but many converge on altered neuronal function.
This section collects additional resources for disease models where functional readouts can support characterization, comparison, and therapeutic testing.
Webinars
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Resources
Application Note with CRL and bit.bio
Developing next-generation in-vitro phenotypic assays for Huntington's disease by combining precision reprogrammed hiPSC-derived disease models with high-density microelectrode arrays.
Publications
Human iPSC-derived glutamatergic neurons with pathogenic KCNQ2 variants display hyperactive bursting phenotypes
Multiplex epigenome editing of MECP2 to rescue Rett syndrome neurons
Conferences
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Dr. Maria Sundberg
“To identify the molecular pathways that are causing the disease phenotypes in these neurons we have studied their network functions on MaxWell Biosystems HD-MEA, gene expression, profiles with RNA sequencing, and synaptic marker expression profiles using immunocytochemical assays. The multi-well platform allows us to record from several wells/conditions at the same time. This is helpful when comparing the network function between control and patient cell populations.”
Dr. Danny McSweeney
“Our team is using the MaxOne HD-MEA System to probe neuronal network synchrony for human induced cortical excitatory neurons across genetic backgrounds. Changes in bursting patterns between wild-type and CASK-knockout genotypes manifest through severe deficits in neuronal burst frequency, mean spikes per burst, and mean inter-burst intervals. To investigate these changes, the MaxOne HD-MEA System provides us an easy, straightforward, and user-friendly system.”
