ArticleMolecular neurobiology2019
Amyloid β Peptide Compromises Neural Stem Cell Fate by Irreversibly Disturbing Mitochondrial Oxidative State and Blocking Mitochondrial Biogenesis and Dynamics.
Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Mitochondrial dynamics and function in neural differentiation: a systematic review.European journal of medical research · 2025Pooled it
- Mitochondrial Fusion and Fission in Age-Related Cardio-Cerebral Diseases: Mechanisms and Interventions.Aging cell · 2026Review
- BDNF-Hyaluronic Acid Hydrogel Promotes Neuronal Differentiation of Neural Stem Cells in Aβ-Induced Injury and 5×FAD Mice.Biomedicines · 2026Article
- Asparagine Deamidation Attenuates Toxicity, Aggregation, and Microglial Responses of Alzheimer's Amyloid-β.ACS chemical neuroscience · 2025Article
- Mitochondrial sirtuins, key regulators of aging.Life medicine · 2025Review
- Neural stem cells fate under neuroinflammatory conditions and oxidative stress response.Frontiers in cellular neuroscience · 2025Review
- The relationship between adult hippocampal neurogenesis and cognitive impairment in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Review
- Rational fusion design inspired by cell-penetrating peptide: SS31/S-14 G Humanin hybrid peptide with amplified multimodal efficacy and bio-permeability for the treatment of Alzheimer's disease.Asian journal of pharmaceutical sciences · 2024Article
- Comprehensive characterization of the neurogenic and neuroprotective action of a novel TrkB agonist using mouse and human stem cell models of Alzheimer's disease.Stem cell research & therapy · 2024Article
- Review
- Pharmacological Inhibition of the Asparaginyl Endopeptidase (AEP) in an Alzheimer's Disease Model Improves the Survival and Efficacy of Transplanted Neural Stem Cells.International journal of molecular sciences · 2023Article
- Apigenin attenuates LPS-induced neurotoxicity and cognitive impairment in mice via promoting mitochondrial fusion/mitophagy: role of SIRT3/PINK1/Parkin pathway.Psychopharmacology · 2022Article
- Sirt3 deficiency induced down regulation of insulin degrading enzyme in comorbid Alzheimer's disease with metabolic syndrome.Scientific reports · 2022Article
- Aberrant Energy Metabolism in Alzheimer's Disease.Journal of translational internal medicine · 2022Article
- Brain endothelium-derived extracellular vesicles containing amyloid-beta induce mitochondrial alterations in neural progenitor cells.Extracellular vesicles and circulating nucleic acids · 2022Article
- Sirtuin 3 (SIRT3) Pathways in Age-Related Cardiovascular and Neurodegenerative Diseases.Biomedicines · 2021Review
- Review
- Ginkgolide B‑induced AMPK pathway activation protects astrocytes by regulating endoplasmic reticulum stress, oxidative stress and energy metabolism induced by Aβ1‑42.Molecular medicine reports · 2021Article
- Article
- Acupuncture accelerates neural regeneration and synaptophysin production after neural stem cells transplantation in mice.World journal of stem cells · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is the most common neurodegenerative disease and is characterized by the accumulation of amyloid β peptide (Aβ). Although most AD mouse models present a decline in neurogenesis, they express mutated genes which regulate neurogenesis per se and are not present in most AD patients, thus masking the real impact of Aβ on adult neurogenesis. Mitochondrion, a well-known target of Aβ in neurons, is a main regulator of neural stem cell (NSC) fate. Here, we aimed to investigate the impact of Aβ on NSC mitochondria and cell fate decisions, namely whether and how Aβ affects neurogenesis. NSC fate and mitochondrial parameters, including biogenesis, dynamics, and oxidative stress, were evaluated. Our results showed that Aβ impaired NSC viability and proliferation and indirectly blocked neurogenic differentiation, by disrupting mitochondrial signaling of self-renewing NSCs. Importantly, Aβ decreased ATP levels, generated oxidative stress, and affected the radical scavenger system through SOD2 and SIRT3. Aβ also reduced mtDNA and mitochondrial biogenesis proteins, such as Tfam, PGC-1α, and NRF1, and inhibited activation of PGC-1α-positive regulator CREB. Moreover, Aβ triggered mitochondrial fragmentation in self-renewing NSCs and reduced mitochondrial fusion proteins, such as Mfn2 and ERRα. Notably, Aβ compromised NSC commitment and survival by irreversibly impairing mitochondria and thwarting any neurogenic rescue through mitochondrial biogenesis, dynamics, or radical scavenger system. Altogether, this study brings new perspective to rethink the molecular targets relevant for endogenous NSC-based strategies in AD.
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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.