ArticleAging and disease2022
Locomotor Hyperactivity in the Early-Stage Alzheimer's Disease-like Pathology of APP/PS1 Mice: Associated with Impaired Polarization of Astrocyte Aquaporin 4.
Article in Aging and disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it.
- A systematic review of exposure to endocrine disruptors and energy expenditure in mice.Environmental health : a global access science source · 2025Pooled it
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- Age-Associated Behavioral Alterations in Laboratory-Housed Octodon degus.bioRxiv : the preprint server for biology · 2026Article
- Early glymphatic failure in AppNL-F knock-in mice is linked to parenchymal border macrophages loss.Brain : a journal of neurology · 2026Article
- Behavioral and brain-wide neural signatures of sundowning in Alzheimer's disease.Research square · 2026Article
- Sex- and age-dependent mitochondrial dysfunction and cognitive impairment in a mouse model of familial hypercholesterolemia.Biology of sex differences · 2026Article
- Exercise-induced modulation of astrocyte in Alzheimer's disease: mechanisms and therapeutic implications.Frontiers in physiology · 2026Review
- Repeated Exposure to Lidocaine Induces Alzheimer's‐Like Cognitive Impairment and Neuropathology in Aged Mice Through BDNF‐Regulated Autophagy.Journal of cellular and molecular medicine · 2025Article
- Trifluoperazine improves postoperative cognition by influencing astrocyte endfoot morphology and aquaporin-4 polarity.Molecular neurobiology · 2025Article
- Characterization of adult hippocampal neurogenesis in the novelbioRxiv : the preprint server for biology · 2025Article
- Particulate matter and co-occurring genetic risk induce oxidative stress and cardiac and brain Alzheimer's pathology.Communications biology · 2025Article
- Caspase-12 is Expressed in Purkinje Neurons and Prevents Psychiatric-Like Behavior in Mice.Molecular neurobiology · 2025Article
- Novel mouse model of Alzheimer's disease exhibits pathology through synergistic interactions among amyloid-β, tau, and reactive astrogliosis.Zoological research · 2025Article
- Mutation inFrontiers in neuroscience · 2025Article
- NOTCH3 Mutation Causes Glymphatic Impairment and Promotes Brain Senescence in CADASIL.CNS neuroscience & therapeutics · 2025Article
- Upregulation of Na/H Exchanger in Astrogliosis and Early Alzheimer's Disease Pathogenesis.Aging and disease · 2024Article
- Transport of β-amyloid from brain to eye causes retinal degeneration in Alzheimer's disease.The Journal of experimental medicine · 2024Article
- Knockdown of microglial iron import gene, Slc11a2, worsens cognitive function and alters microglial transcriptional landscape in a sex-specific manner in the APP/PS1 model of Alzheimer's disease.Journal of neuroinflammation · 2024Article
- Hepatic LRP-1 plays an important role in amyloidosis in Alzheimer's disease mice: Potential role in chronic heavy alcohol feeding.Neurobiology of disease · 2024Article
- Knockdown of microglial iron import gene, DMT1, worsens cognitive function and alters microglial transcriptional landscape in a sex-specific manner in the APP/PS1 model of Alzheimer's disease.Research square · 2024Article
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Authors and funding
15 authors.
Funding
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Abstract
Non-cognitive behavioral and psychological symptoms often occur in Alzheimer's disease (AD) patients and mouse models, although the exact neuropathological mechanism remains elusive. Here, we report hyperactivity with significant inter-individual variability in 4-month-old APP/PS1 mice. Pathological analysis revealed that intraneuronal accumulation of amyloid-β (Aβ), c-Fos expression in glutamatergic neurons and activation of astrocytes were more evident in the frontal motor cortex of hyperactive APP/PS1 mice, compared to those with normal activity. Moreover, the hyperactive phenotype was associated with mislocalization of perivascular aquaporin 4 (AQP4) and glymphatic transport impairment. Deletion of the AQP4 gene increased hyperactivity, intraneuronal Aβ load and glutamatergic neuron activation, but did not influence working memory or anxiety-like behaviors of 4-month-old APP/PS1 mice. Together, these results demonstrate that AQP4 mislocalization or deficiency leads to increased intraneuronal Aβ load and neuronal hyperactivity in the motor cortex, which in turn causes locomotor over-activity during the early pathophysiology of APP/PS1 mice. Therefore, improving AQP4 mediated glymphatic clearance may offer a new strategy for early intervention of hyperactivity in the prodromal phase of AD.
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