ReviewFrontiers in cellular neuroscience2015
Gene expression parallels synaptic excitability and plasticity changes in Alzheimer's disease.
Review in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- Pooled it
- Pyrazole-derived TRPC3 antagonist ameliorates synaptic dysfunctions and memory deficits in Alzheimer's disease models.Molecular psychiatry · 2026Article
- Astrocyte activation persists one year after TBI: a dynamic shift from inflammation to neurodegeneration.Communications biology · 2025Article
- Neuronal gene profiling of tau oligomer-bearing cholinergic nucleus basalis neurons during the onset of Alzheimer's disease.Acta neuropathologica communications · 2025Article
- miR-361-5p contributes to the pathogenesis of Alzheimer's disease.Scientific reports · 2025Article
- Cerebrospinal fluid cyclase-associated protein 2 is increased in Alzheimer's disease and correlates with tau pathology.Translational neurodegeneration · 2025Article
- Machine Learning and Digital Biomarkers Can Detect Early Stages of Neurodegenerative Diseases.Sensors (Basel, Switzerland) · 2024Review
- Article
- Compensatory remodeling of a septo-hippocampal GABAergic network in the triple transgenic Alzheimer's mouse model.Journal of translational medicine · 2023Article
- Glial cell transcriptome analyses in 3xTg-AD mice: Effects of aging, disease progression, and anti-Aβ immunotherapy.Aging brain · 2023Article
- Astrocyte contribution to dysfunction, risk and progression in neurodegenerative disorders.Nature reviews. Neuroscience · 2023Review
- Spatial Memory Training Counteracts Hippocampal GIRK Channel Decrease in the Transgenic APPInternational journal of molecular sciences · 2022Article
- Pridopidine Promotes Synaptogenesis and Reduces Spatial Memory Deficits in the Alzheimer's Disease APP/PS1 Mouse Model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- Identification of Therapeutic Targets for Amyotrophic Lateral Sclerosis Using PandaOmics - An AI-Enabled Biological Target Discovery Platform.Frontiers in aging neuroscience · 2022Article
- Changes in the brain transcriptome after DNA Aβ42 trimer immunization in a 3xTg-AD mouse model.Neurobiology of disease · 2021Article
- Synaptic and metabolic gene expression alterations in neurons that are recipients of proteopathic tau seeds.Acta neuropathologica communications · 2020Article
- Human iPSC-Derived Hippocampal Spheroids: An Innovative Tool for Stratifying Alzheimer Disease Patient-Specific Cellular Phenotypes and Developing Therapies.Stem cell reports · 2020Article
- GenEpi: gene-based epistasis discovery using machine learning.BMC bioinformatics · 2020Article
- Early Long-Term Memory Impairment and Changes in the Expression of Synaptic Plasticity-Associated Genes, in the McGill-R-Thy1-APP Rat Model of Alzheimer's-Like Brain Amyloidosis.Frontiers in aging neuroscience · 2020Article
- Identification of age- and gender-associated long noncoding RNAs in the human brain with Alzheimer's disease.Neurobiology of aging · 2019Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by abnormal accumulation of β-amyloid and tau and synapse dysfunction in memory-related neural circuits. Pathological and functional changes in the medial temporal lobe, a region essential for explicit memory encoding, contribute to cognitive decline in AD. Surprisingly, functional imaging studies show increased activity of the hippocampus and associated cortical regions during memory tasks in presymptomatic and early AD stages, whereas brain activity declines as the disease progresses. These findings suggest an emerging scenario where early pathogenic events might increase neuronal excitability leading to enhanced brain activity before clinical manifestations of the disease, a stage that is followed by decreased brain activity as neurodegeneration progresses. The mechanisms linking pathology with synaptic excitability and plasticity changes leading to memory loss in AD remain largely unclear. Recent studies suggest that increased brain activity parallels enhanced expression of genes involved in synaptic transmission and plasticity in preclinical stages, whereas expression of synaptic and activity-dependent genes are reduced by the onset of pathological and cognitive symptoms. Here, we review recent evidences indicating a relationship between transcriptional deregulation of synaptic genes and neuronal activity and memory loss in AD and mouse models. These findings provide the basis for potential clinical applications of memory-related transcriptional programs and their regulatory mechanisms as novel biomarkers and therapeutic targets to restore brain function in AD and other cognitive disorders.
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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.