GABAergic Interneuron Dysfunction Impairs Hippocampal Neurogenesis in Adult Apolipoprotein E4 Knockin Mice
Open accessAbstract
Apolipoprotein (apo) E, a polymorphic protein with three isoforms (apoE2, apoE3, and apoE4), is essential for lipid homeostasis. Carriers of apoE4 are at higher risk for developing Alzheimer's disease. We have investigated adult neurogenesis in mice with knockout (KO) for apoE or with knockin (KI) alleles for human apoE3 or apoE4, and we report that neurogenesis is reduced in both apoE-KO and apoE4-KI mice. In apoE-KO mice, increased BMP signaling promoted glial differentiation at the expense of neurogenesis. In contrast, in apoE4-KI mice, presynaptic GABAergic input-mediated maturation of newborn neurons was diminished. Tau phosphorylation, an Alzheimer's disease characteristic, and levels of neurotoxic apoE fragments were both elevated in apoE4-KI hippocampal neurons concomitant with decreased GABAergic interneuron survival. Potentiating GABAergic signaling restored neuronal maturation and neurogenesis in apoE4-KI mice to normal levels. These findings suggest that GABAergic signaling can be targeted to mitigate the deleterious effects of apoE4 on neurogenesis.
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APOE4 exacerbates AD-related pathologies, including amyloid-beta plaques, Tau tangles, neurodegeneration and neuroinflammation.
“It exacerbates AD-related pathologies, including amyloid-beta (Aβ) plaques, Tau tangles, neurodegeneration and neuroinflammation4–16.”
From The APOE-R136S mutation protects against APOE4-driven tau pathology, neurodegeneration, and neuroinflammation (2023) · cites this paper as [10]
The Results report increased tau phosphorylation and reduced neuronal survival in apoE4 knock-in mouse cultures; the Discussion links apoE4 neurotoxicity to neurodegeneration and describes a pathway to neurofibrillary tangles (page numbers unavailable). The passages do not establish that APOE4 exacerbates amyloid-beta plaques or neuroinflammation, and the study measures tau phosphorylation rather than tangle burden. (LLM, conf=0.88)
Experimental — accuracy not yet measuredNeurogenesis is known to be elevated following hyperexcitability.
“Among the downregulated pathways in E3S/S/P301S hippocampus, neurogenesis is known to be elevated following hyperexcitability58,59, observed in E3/P301S mice using cFOS activity mapping.”
From The R136S mutation in the APOE3 gene confers resilience against tau pathology via inhibition of the cGAS-STING-IFN pathway (2025) · cites this paper as [58]
The Results section on GABAA receptor manipulation reports increased newborn-cell proliferation when GABA signaling was inhibited. But the Results section on GABAergic interneurons describes impaired neuronal maturation in that setting, and the paper does not establish that hyperexcitability elevates overall neurogenesis. Page numbers are unavailable in our copy. (LLM, conf=0.82)
Experimental — accuracy not yet measuredNeurogenesis is elevated in response to hyperexcitability.
“Neurogenesis is known to be elevated in response to hyperexcitability53,54”
From <i>APOE3</i> - <i>R136S</i> mutation confers resilience against tau pathology via cGAS-STING-IFN inhibition (2024) · cites this paper as [53]
The Results section on GABAA receptor treatment reports increased newborn-cell proliferation after reduced GABA signaling, but does not establish hyperexcitability or show that it elevates neurogenesis. The Discussion addresses GABAergic excitation in newborn-neuron maturation, not neurogenesis as a response to hyperexcitability. Searches for hyperexcitability, seizures, and increased neuronal activity found no passage making the attributed claim; page numbers were unavailable in our copy. (LLM, conf=0.72)
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- Authors
- Li, G., Bien-Ly, N., Andrews-Zwilling, Y., Xu, Q., Bernardo, A., Ring, K., Halabisky, B., Deng, C., Mahley, R. W., & Huang, Y.
- Affiliations
- Gladstone Institutes (US)
- University of California, San Francisco (US)
- Corresponding author
- Huang, Yadong
- Venue
- Cell Stem Cell
- Publisher
- Elsevier BV
- Published
- 2009-12
- Volume
- 5
- Issue
- 6
- Pages
- 634-645
- ISSN
- 1875-9777 (ISSN-L)
- 1934-5909
- PMC
- PMC2992822
- OpenAlex
- W2047173060
- Cited by
- 288
- References
- 71
- Citations by year
- 2026: 21 · 2025: 15 · 2024: 21 · 2023: 25 · 2022: 20 · 2021: 15 · 2020: 16 · 2019: 18 · 2018: 11 · 2017: 22 · 2016: 19 · 2015: 14 · 2014: 16 · 2013: 22 · 2012: 11
- FWCI
- 3.45
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell stem cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- California Institute for Regenerative Medicine
- California Institute of Regenerative Medicine
- Gladstone Institutes
- National Institutes of Health
- National Institute on Aging (P01AG022074)
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- APOE ε4, adult hippocampal neurogenesis, GABAergic interneurons, Alzheimer's disease, BMP signaling, glial differentiation, tau phosphorylation, GABAergic neurotransmission, ApoE-deficient mice
- MeSH terms
- Alzheimer Disease, Animals, Animals, Newborn, Apolipoproteins, Cell Differentiation, Hippocampus, Humans, Interneurons, Neuroglia, Signal Transduction, tau Proteins, Mice, Knockout, GABA Agonists, Bone Morphogenetic Proteins, Cell Proliferation, Mice, Adult Stem Cells, Neurogenesis, Gene Knock-In Techniques
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