Mechanisms of hyperexcitability in Alzheimer’s disease hiPSC-derived neurons and cerebral organoids vs isogenic controls
Open accessAbstract
Human Alzheimer’s disease (AD) brains and transgenic AD mouse models manifest hyperexcitability. This aberrant electrical activity is caused by synaptic dysfunction that represents the major pathophysiological correlate of cognitive decline. However, the underlying mechanism for this excessive excitability remains incompletely understood. To investigate the basis for the hyperactivity, we performed electrophysiological and immunofluorescence studies on hiPSC-derived cerebrocortical neuronal cultures and cerebral organoids bearing AD-related mutations in presenilin-1 or amyloid precursor protein vs. isogenic gene corrected controls. In the AD hiPSC-derived neurons/organoids, we found increased excitatory bursting activity, which could be explained in part by a decrease in neurite length. AD hiPSC-derived neurons also displayed increased sodium current density and increased excitatory and decreased inhibitory synaptic activity. Our findings establish hiPSC-derived AD neuronal cultures and organoids as a relevant model of early AD pathophysiology and provide mechanistic insight into the observed hyperexcitability.
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Detecting the expression of Map-2 and NeuN helps determine the extent of neuronal damage and degeneration.
“Map-2 and NeuN are the neuronal marker proteins used to assess the morphology and function of neurons, and detecting the expression of Map-2 and NeuN could help know the extent of neuronal damage and degeneration in the present study (Götz and Ittner, 2008; Ghatak et al., 2019; Sattarov et al., 2023).”
From AD-Like Neuropsychiatric Dysfunction in a Mice Model Induced by a Combination of High-Fat Diet and Intraperitoneal Injection of Streptozotocin (2024) · cites this paper as Ghatak et al., 2019
The Results section reports reduced neurite area in Alzheimer’s disease neurons measured with MAP2 antibody labeling, supporting the use of MAP2 to assess neuronal morphology. The paper’s immunocytochemistry methods list other neuronal markers but not NeuN, and our copy does not show that measuring expression of both MAP2 and NeuN determines the extent of neuronal damage or degeneration. Page numbers are unavailable in our copy. (LLM, conf=0.84)
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Self-citation
- Authors
- Ghatak, S., Dolatabadi, N., Trudler, D., Zhang, X., Wu, Y., Mohata, M., Ambasudhan, R., Talantova, M., & Lipton, S. A.
- Affiliations
- Scripps Research Institute (US)
- Scintillon Institute (US)
- Corresponding author
- Lipton, Stuart A
- ORCID
- Venue
- eLife
- Publisher
- eLife Sciences Publications, Ltd
- Published
- 2019-11-29
- Volume
- 8
- ISSN
- 2050-084X (ISSN-L)
- PMC
- PMC6905854
- OpenAlex
- W2989784226
- Cited by
- 227
- References
- 12
- Citations by year
- 2026: 23 · 2025: 32 · 2024: 27 · 2023: 40 · 2022: 39 · 2021: 50 · 2020: 16
- FWCI
- 17.59
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- eLife (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health (P01 HD29587, DP1 DA041722, R01 NS086890, R01 AG056259, RF1 AG057409)
- National Institute of Neurological Disorders and Stroke (Core grant P30 NS076411)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Keywords
- Alzheimer's disease, neuronal hyperexcitability, hiPSC-derived neurons, brain organoids, presenilin 1 mutations, amyloid precursor protein mutations, sodium current density, synaptic dysfunction, neurite length
- MeSH terms
- Cortical Excitability, Action Potentials, Alzheimer Disease, Animals, Cells, Cultured, Fluorescent Antibody Technique, Humans, Models, Theoretical, Neurons, Organoids, Amyloid beta-Protein Precursor, Cell Size, Mutant Proteins, Mice, Presenilin-1, Cerebrum, Electrophysiological Phenomena, Induced Pluripotent Stem Cells
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