ReviewNeural plasticity2012
Spines, plasticity, and cognition in Alzheimer's model mice.
Review in Neural plasticity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
74 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.
- Transcriptome meta-analysis reveals a central role for sex steroids in the degeneration of hippocampal neurons in Alzheimer's disease.BMC systems biology · 2013Pooled it
- A Novel Nogo-A Receptor Antagonist Peptide Impedes Alzheimer's Disease Pathology by Nogo-A/NgR/ROCK Signaling Pathway.CNS neuroscience & therapeutics · 2026Article
- Selective weakening of population-coupled synaptic activity in vivo in a mouse model of amyloid-beta pathology.Nature communications · 2026Article
- Restoration neurite growth by removing the blockage of endosome trafficking in Alzheimer-like mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Hearing modulation affects Alzheimer's disease progression linked to brain inflammation: a study in mouse models.Molecular medicine (Cambridge, Mass.) · 2024Article
- Alzheimer's disease risk gene CD2AP is a dose-sensitive determinant of synaptic structure and plasticity.Human molecular genetics · 2024Article
- Tau-mediated synaptic dysfunction is coupled with HCN channelopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Reduced Prefrontal-Thalamic Theta Flow During Working Memory Retrieval in APP/PS1 Mice.Journal of Alzheimer's disease : JAD · 2024Article
- Synaptic Compensatory Plasticity in Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Review
- Could theropod dinosaurs have evolved to a human level of intelligence?The Journal of comparative neurology · 2023Review
- The Multifaceted Role of WNT Signaling in Alzheimer's Disease Onset and Age-Related Progression.Cells · 2023Review
- Recent Development in the Understanding of Molecular and Cellular Mechanisms Underlying the Etiopathogenesis of Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Structural synaptic signatures of Alzheimer's disease and dementia with Lewy bodies in the male brain.Neuropathology and applied neurobiology · 2023Article
- Triple-network analysis of Alzheimer's disease based on the energy landscape.Frontiers in neuroscience · 2023Article
- Differential Neuropathology, Genetics, and Transcriptomics in Two Kindred Cases with Alzheimer's Disease and Lewy Body Dementia.Biomedicines · 2022Article
- Structural Plasticity of the Hippocampus in Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- Plasticity in visual cortex is disrupted in a mouse model of tauopathy.Communications biology · 2022Article
- Tuning brain networks: The emerging role of transcranial direct current stimulation on structural plasticity.Frontiers in cellular neuroscience · 2022Review
- Reactive astrocytes: The nexus of pathological and clinical hallmarks of Alzheimer's disease.Ageing research reviews · 2021Review
- FORTIS: a live-cell assay to monitor AMPA receptors using pH-sensitive fluorescence tags.Translational psychiatry · 2021Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
The pathological hallmarks of Alzheimer's disease (AD)--widespread synaptic and neuronal loss and the pathological accumulation of amyloid-beta peptide (Aβ) in senile plaques, as well as hyperphosphorylated tau in neurofibrillary tangles--have been known for many decades, but the links between AD pathology and dementia and effective therapeutic strategies remain elusive. Transgenic mice have been developed based on rare familial forms of AD and frontotemporal dementia, allowing investigators to test in detail the structural, functional, and behavioral consequences of AD-associated pathology. Here, we review work on transgenic AD models that investigate the degeneration of dendritic spine structure, synaptic function, and cognition. Together, these data support a model of AD pathogenesis in which soluble Aβ initiates synaptic dysfunction and loss, as well as pathological changes in tau, which contribute to both synaptic and neuronal loss. These changes in synapse structure and function as well as frank synapse and neuronal loss contribute to the neural system dysfunction which causes cognitive deficits. Understanding the underpinnings of dementia in AD will be essential to develop and evaluate therapeutic approaches for this widespread and devastating disease.
Indexed as
Identifiers
What OpenQuestion holds
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.