ArticleJournal of neuropathology and experimental neurology2013
Dendritic spine density, morphology, and fibrillar actin content surrounding amyloid-β plaques in a mouse model of amyloid-β deposition.
Article in Journal of neuropathology and experimental neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Homomeric and Heteromeric α7 Nicotinic Acetylcholine Receptors in Health and Some Central Nervous System Diseases.Membranes · 2021Review
- Plaque-Associated Oligomeric Amyloid-Beta Drives Early Synaptotoxicity in APP/PS1 Mice Hippocampus: Ultrastructural Pathology Analysis.Frontiers in neuroscience · 2021Article
- The Amyloid-Tau-Neuroinflammation Axis in the Context of Cerebral Amyloid Angiopathy.International journal of molecular sciences · 2019Review
- Density of small dendritic spines and microtubule-associated-protein-2 immunoreactivity in the primary auditory cortex of subjects with schizophrenia.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Article
- Fibrinogen Induces Microglia-Mediated Spine Elimination and Cognitive Impairment in an Alzheimer's Disease Model.Neuron · 2019Article
- Effects of rising amyloidβ levels on hippocampal synaptic transmission, microglial response and cognition in APPEBioMedicine · 2019Article
- Loss of precuneus dendritic spines immunopositive for spinophilin is related to cognitive impairment in early Alzheimer's disease.Neurobiology of aging · 2017Article
- Early Activation of Experience-Independent Dendritic Spine Turnover in a Mouse Model of Alzheimer's Disease.Cerebral cortex (New York, N.Y. : 1991) · 2017Article
- Microglia limit the expansion of β-amyloid plaques in a mouse model of Alzheimer's disease.Molecular neurodegeneration · 2017Article
- Stereological Assessments of Neuronal Pathology in Auditory Cortex in Schizophrenia.Frontiers in neuroanatomy · 2017Review
- Trim9 Deletion Alters the Morphogenesis of Developing and Adult-Born Hippocampal Neurons and Impairs Spatial Learning and Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Corticotropin-releasing factor receptor-1 antagonism mitigates beta amyloid pathology and cognitive and synaptic deficits in a mouse model of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2016Article
- Developmental Trajectories of Auditory Cortex Synaptic Structures and Gap-Prepulse Inhibition of Acoustic Startle Between Early Adolescence and Young Adulthood in Mice.Cerebral cortex (New York, N.Y. : 1991) · 2016Article
- Regulation of the Postsynaptic Compartment of Excitatory Synapses by the Actin Cytoskeleton in Health and Its Disruption in Disease.Neural plasticity · 2016Review
- Oridonin Attenuates Synaptic Loss and Cognitive Deficits in an Aβ1-42-Induced Mouse Model of Alzheimer's Disease.PloS one · 2016Article
- Aβ42-oligomer Interacting Peptide (AIP) neutralizes toxic amyloid-β42 species and protects synaptic structure and function.Scientific reports · 2015Article
- Loss of Microtubule-Associated Protein 2 Immunoreactivity Linked to Dendritic Spine Loss in Schizophrenia.Biological psychiatry · 2015Article
- The hypothalamus in Alzheimer's disease: a Golgi and electron microscope study.American journal of Alzheimer's disease and other dementias · 2015Article
- Analyzing dendritic spine pathology in Alzheimer's disease: problems and opportunities.Acta neuropathologica · 2015Review
- Commentary: is Alzheimer's disease uniquely human?Neurobiology of aging · 2015Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Dendritic spines are the site of most excitatory synapses, the loss of which correlates with cognitive impairment in patients with Alzheimer disease. Substantial evidence indicates that amyloid-β (Aβ) peptide, either insoluble fibrillar Aβ deposited into plaques or soluble nonfibrillar Aβ species, can cause spine loss but the concurrent contributions of fibrillar Aβ and nonfibrillar Aβ to spine loss has not been previously assessed. We used multiple-label immunohistochemistry to measure spine density, size, and F-actin content surrounding plaques in the cerebral cortex in the PSAPP mouse model of Aβ deposition. Our approach allowed us to measure fibrillar Aβ plaque content and an index of nonfibrillar Aβ species concurrently. We found that spine density was reduced within 6 μm of the plaque perimeter, remaining spines were more compact, and F-actin content per spine was increased. Measures of fibrillar Aβ plaque content were associated with reduced spine density near plaques, whereas measures of nonfibrillar Aβ species were associated with reduced spine density and size but not altered F-actin content. These findings suggest that strategies to preserve dendritic spines in AD patients may need to address both nonfibrillar and fibrillar forms of Aβ and that nonfibrillar Aβ may exert spine toxicity through pathways not mediated by depolymerization of F-actin.
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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.