Imbalance between GABAergic and glutamatergic transmission impairs adult neurogenesis in an animal model of Alzheimer’s Disease.

Sun, Binggui; Halabisky, Brian; Zhou, Yungui; Palop, Jorge J.; Yu, Guiqiu; Mucke, Lennart; Gan, Li

doi:10.1016/j.stem.2009.10.003

Cited by 205Neurogenesis and neuroplasticity mechanismsAlzheimer's disease research and treatmentsNeuroscience and Neuropharmacology Research

Imbalance between GABAergic and glutamatergic transmission impairs adult neurogenesis in an animal model of Alzheimer’s Disease.

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Sun, Binggui, Halabisky, Brian, Zhou, Yungui, Palop, Jorge J., Yu, Guiqiu, Mucke, Lennart, Gan, Li·2009·Cell Stem Cell

DOI 10.1016/j.stem.2009.10.003PMC PMC2823799

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Abstract

Adult neurogenesis regulates plasticity and function in the hippocampus, which is critical for memory and vulnerable to Alzheimer's disease (AD). Promoting neurogenesis may improve hippocampal function in AD brains. However, how amyloid beta (Abeta), the key AD pathogen, affects the development and function of adult-born neurons remains unknown. Adult-born granule cells (GCs) in human amyloid precursor protein (hAPP) transgenic mice, an AD model, showed greater dendritic length, spine density, and functional responses than did controls early in development, but were impaired morphologically and functionally during later maturation. Early inhibition of GABA(A) receptors to suppress GABAergic signaling or late inhibition of calcineurin to enhance glutamatergic signaling normalized the development of adult-born GCs in hAPP mice with high Abeta levels. Abeta-induced increases in GABAergic neurotransmission or an imbalance between GABAergic and glutamatergic neurotransmission may contribute to impaired neurogenesis in AD.

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Perineuronal net loss in AD may contribute to altered E/I balance.
“Perineuronal net loss in AD may contribute to altered E/I balance (Palop et al., 2007; Sun et al., 2009)”
From The Perineuronal ‘Safety’ Net? Perineuronal Net Abnormalities in Neurological Disorders (2018) · cites this paper as Sun et al., 2009
For proper functioning of neurons, there should be a critical balance between excitatory and inhibitory neurotransmitters.
“Furthermore, it has been established that for the proper functioning of neurons, there should be a critical balance between the excitatory and inhibitory neurotransmitters [155,156,157,158].”
From Acetylcholinesterase Inhibitory Potential of Various Sesquiterpene Analogues for Alzheimer’s Disease Therapy (2021) · cites this paper as [157]

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Authors: Sun, B., Halabisky, B., Zhou, Y., Palop, J. J., Yu, G., Mucke, L., & Gan, L.
Affiliations: University of California, San Francisco (US)
Corresponding author: Gan, Li
ORCID: Sun, Binggui
Palop, Jorge J.
Mucke, Lennart
Gan, Li
Venue: Cell Stem Cell
Publisher: Elsevier BV
Published: 2009-12
Volume: 5
Issue: 6
Pages: 624-633
ISSN: 1875-9777 (ISSN-L)
1934-5909
DOI: 10.1016/j.stem.2009.10.003
PMC: PMC2823799
OpenAlex: W2016632386
Cited by: 205
References: 52
Citations by year: 2026: 3 · 2025: 8 · 2024: 16 · 2023: 10 · 2022: 26 · 2021: 16 · 2020: 10 · 2019: 10 · 2018: 13 · 2017: 6 · 2016: 19 · 2015: 7 · 2014: 17 · 2013: 14 · 2012: 10
FWCI: 3.14
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 1324 d)
Locations: Cell stem cell (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health (1c06rr018928-01)
National Institute on Aging (P01AG004342, AG022074, P01AG022074)
National Cancer Institute (CO6 RRO18928)
National Institute of Neurological Disorders and Stroke (R01NS041787, NS041787)
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: adult neurogenesis, Alzheimer's disease, amyloid-beta, GABAergic neurotransmission, glutamatergic neurotransmission, GABAA receptor, calcineurin, hippocampus, dendritic spine development, neuronal maturation
MeSH terms: Alzheimer Disease, Animals, Cell Differentiation, Disease Models, Animal, Hippocampus, Humans, Mice, Transgenic, Synaptic Transmission, Amyloid beta-Peptides, Neurites, Tacrolimus, Pertussis Toxin, Dendritic Spines, Mice, Neurogenesis, GABA-A Receptor Antagonists, Calcineurin Inhibitors

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Imbalance between GABAergic and glutamatergic transmission impairs adult neurogenesis in an animal model of Alzheimer’s Disease.

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