ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Wild-type neural progenitors divide and differentiate normally in an amyloid-rich environment.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- Neuronal subtype governs amyloid structure, cellular response, and cognitive outcome in genetically targeted APP mouse models.Molecular neurodegeneration · 2026Article
- Adult hippocampal neurogenesis: New avenues for treatment of brain disorders.Stem cell reports · 2025Review
- AIMP2 accumulation in brain leads to cognitive deficits and blood secretion in Parkinson's disease.Journal of translational medicine · 2024Article
- Hippocampal neurogenesis and pro-neurogenic therapies for Alzheimer's disease.Animal models and experimental medicine · 2022Review
- Implication of Adult Hippocampal Neurogenesis in Alzheimer's Disease and Potential Therapeutic Approaches.Cells · 2022Review
- Treadmill Exercise Ameliorates Adult Hippocampal Neurogenesis Possibly by Adjusting the APP Proteolytic Pathway in APP/PS1 Transgenic Mice.International journal of molecular sciences · 2021Article
- Emergence of synaptic and cognitive impairment in a mature-onset APP mouse model of Alzheimer's disease.Acta neuropathologica communications · 2019Article
- Oligomer-prone E57K-mutant alpha-synuclein exacerbates integration deficit of adult hippocampal newborn neurons in transgenic mice.Brain structure & function · 2018Article
- Exosomes Secreted from HEK293-APP Swe/Ind Cells Impair the Hippocampal Neurogenesis.Neurotoxicity research · 2017Article
- High-resolution bioelectrical imaging of Aβ-induced network dysfunction on CMOS-MEAs for neurotoxicity and rescue studies.Scientific reports · 2017Article
- Altered neurogenesis in mouse models of Alzheimer disease.Neurogenesis (Austin, Tex.) · 2017Review
- Sex-related dimorphism in dentate gyrus atrophy and behavioral phenotypes in an inducible tTa:APPsi transgenic model of Alzheimer's disease.Neurobiology of disease · 2016Article
- Amyloid β Is Not the Major Factor Accounting for Impaired Adult Hippocampal Neurogenesis in Mice Overexpressing Amyloid Precursor Protein.Stem cell reports · 2016Article
- Neural stem/progenitor cells in Alzheimer's disease.The Yale journal of biology and medicine · 2016Review
- Article
- Insights into the physiological function of the β-amyloid precursor protein: beyond Alzheimer's disease.Journal of neurochemistry · 2014Review
- Reconsidering hippocampal neurogenesis in Alzheimer's disease.Frontiers in neuroscience · 2014Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Adult neurogenesis is modulated by a balance of extrinsic signals and intrinsic responses that maintain production of new granule cells in the hippocampus. Disorders that disrupt the proliferative niche can impair this process, and alterations in adult neurogenesis have been described in human autopsy tissue and transgenic mouse models of Alzheimer's disease. Because exogenous application of aggregated Aβ peptide is neurotoxic in vitro and extracellular Aβ deposits are the main pathological feature recapitulated by mouse models, cell-extrinsic effects of Aβ accumulation were thought to underlie the breakdown of hippocampal neurogenesis observed in Alzheimer's models. We tested this hypothesis using a bigenic mouse in which transgenic expression of APP was restricted to mature projection neurons. These mice allowed us to examine how wild-type neural progenitor cells responded to high levels of Aβ released from neighboring granule neurons. We find that the proliferation, determination, and survival of hippocampal adult-born granule neurons are unaffected in the APP bigenic mice, despite abundant amyloid pathology and robust neuroinflammation. Our findings suggest that Aβ accumulation is insufficient to impair adult hippocampal neurogenesis, and that factors other than amyloid pathology may account for the neurogenic deficits observed in transgenic models with more widespread APP expression.
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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 OpenQuestion graph.