ArticleOncotarget2017
Motor deficits are independent of axonopathy in an Alzheimer's disease mouse model of TgCRND8 mice.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Motor performance and its association with Alzheimer's-related biomarkers: a systematic review.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Pooled it
- Alzheimer's Disease: Understanding Motor Impairments.Brain sciences · 2024Review
- p17/C18-ceramide-mediated mitophagy is an endogenous neuroprotective response in preclinical and clinical brain injury.PNAS nexus · 2024Article
- Effects and mechanisms of APP and its cleavage product Aβ in the comorbidity of sarcopenia and Alzheimer's disease.Frontiers in aging neuroscience · 2024Review
- Serum amyloid P component accumulates and persists in neurones following traumatic brain injury.Open biology · 2023Article
- Assessments of prolonged effects of desflurane and sevoflurane on motor learning deficits in aged AppMolecular brain · 2022Article
- Age Related Changes in Muscle Mass and Force Generation in the Triple Transgenic (3xTgAD) Mouse Model of Alzheimer's Disease.Frontiers in aging neuroscience · 2022Article
- Established Beta Amyloid Pathology Is Unaffected by TREM2 Elevation in Reactive Microglia in an Alzheimer's Disease Mouse Model.Molecules (Basel, Switzerland) · 2021Article
- Origins of Beta Amyloid Differ Between Vascular Amyloid Deposition and Parenchymal Amyloid Plaques in the Spinal Cord of a Mouse Model of Alzheimer's Disease.Molecular neurobiology · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There have been an increasing number of reports of non-cognitive symptoms in Alzheimer's disease (AD). Some symptoms are associated with the loss of motor functions, e.g. gait disturbances, disturbed activity level and balance. Consistent with clinical findings, several AD mouse models harboring amyloid pathology develop motor impairment. Although the factors that contribute to the motor deficits have not yet been determined, it has been suggested that axonopathy is one of the key factors that may contribute to this particular feature of the disease. Our previous study found that TgCRND8 mice exhibited profound motor deficits as early as 3 months old. In this study, we explored the possible factors that may be related to motor deficits in TgCRND8 mice. Results from silver, neurofilament and amyloid precursor protein (APP) staining revealed no axonopathy occurred in the brain and spinal cord of TgCRND8 mice at the age of 3 months. Anterograde labeling of corticospinal tract of spinal cord and electronic microscopy (EM) analysis showed that no axonopathy occurred in TgCRND8 mice at the age of 3 months. According to these results, it could be concluded that no axonal alterations were evident in the TgCRND8 mice when motor deficits was overt. Thus, axonopathy may play a less prominent role in motor deficits in AD. These results suggest that mechanisms by which motor function undergo impairment in AD need to be further studied.
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