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plasticity
288 studies tagged plasticity, dated 1983-02-20 to 2026-10-29. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- Aβ42 oligomers disrupt calcium homeostasis via Piezo1 and induce neurotoxicity in differentiated SH-SY5Y cells 2026-10-29
- Endocannabinnoids innervate Circadian mechinary mitigating neuroinflammation, amyloidogenesis and cognition phenotypic to AD 2026-10-29
- Repeated VU0155069 Treatment Is Associated with Region- and Pathological Stage-Specific Dendritic Spine Remodeling in Female 3xTg-AD Mice 2026-10-27
Studies
288 studies carry this tag.
Date range
1983 to 2026
Top journals
- The Journal of neuroscience : the official journal of the Society for Neuroscience 17
- Nature neuroscience 10
- Neuron 10
- bioRxiv 10
- Nature 8
137 journals in all.
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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39/100
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by Aβ-driven synaptic dysfunction in the early phases of pathogenesis.
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Mus treatment attenuated memory dysfunction, reduced Aβ level, and enhanced synaptic plasticity in APP/PS1 mice.
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The postsynaptic density (PSD) is a complex subcellular domain important for postsynaptic signaling, function, and plasticity.
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Long-term potentiation (LTP) and long-term depression (LTD) of hippocampal synaptic transmission represent the principal experimental models underlying learning and memory.
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38/100
We previously reported that inducing gamma oscillations with a non-invasive light flicker (gamma entrainment using sensory stimulus or GENUS) impacted pathology in the visual cortex of Alzheimer's disease mouse models.
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In Alzheimer's disease (AD), early synaptic dysfunction is associated with the increased oligomeric amyloid-beta peptide, which causes NMDAR-dependent synaptic depression and spine elimination.
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Astrocytes serve important roles that affect recruitment and function of neurons at the local and network levels.
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Dendritic spines are small, thin, specialized protrusions from neuronal dendrites, primarily localized in the excitatory synapses.
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47/100
Defective brain hormonal signaling has been associated with Alzheimer's disease (AD), a disorder characterized by synapse and memory failure.
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In BriefIn the search for biomarkers of synapse loss associated with Alzheimer's disease (AD), we used shotgun proteomics to identify a panel of 9 synaptic proteins detectable in human cerebrospinal fluid (CSF).Expression at the human synapse was verified using super resolution microscopy.
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Neuromodulation regulates critical functions of CNS synapses, ranging from neural circuit development to high-order cognitive processes, including learning and memory.
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39/100
Dozens of genes have been implicated in late onset Alzheimer's disease (AD) risk, but none has a defined mechanism of action in neurons.
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The dosage of the serine threonine kinase DYRK1A is critical in the central nervous system (CNS) during development and aging.
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To demonstrate this hypothesis, we established abnormalities in the glucose metabolism utilizing thiamine deficiency in vitro and in vivo, and we found dramatically reduced dendrite spine density.
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Alzheimer's disease (AD) represents a major healthcare burden with no effective treatment.
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Microribonucleic acids (miRNAs) play a pivotal role in numerous aspects of the nervous system and are increasingly recognized as key regulators in neurodegenerative diseases.
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Klotho, encoded by the KL gene, is a single-pass transmembrane protein and a circulating factor that plays a key role in cellular metabolism and body homeostasis and has been associated with age-related diseases.
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Alzheimer's disease (AD) is emerging as a synaptopathology driven by metaplasticity.
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Amyloid pathology occurs early in Alzheimer's disease (AD), and has therefore been the focus of numerous studies.
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Early-stage Alzheimer's disease is characterized by the loss of dendritic spines in the neocortex of the brain.
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Synaptic plasticity is a cellular process involved in learning and memory whose alteration in its two main forms (Long Term Depression (LTD) and Long Term Potentiation (LTP)), is observed in most brain pathologies, including neurodegenerative disorders such as Alzheimer's disease (AD).
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Stress is critically involved in the development and progression of disease.
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Alzheimer's disease (AD) is a neurodegenerative pathology characterized by aggregates of amyloid-β (Aβ) and phosphorylated tau protein, synaptic dysfunction, and spatial memory impairment.
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39/100
Genetically modified mice have provided insights into the progression and pathology of Alzheimer's disease (AD).
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Alzheimer'sdisease(AD) is characterized by deposition of amyloid-β (Aβ)plaques, neurofibrillary tangles, andneuronal loss, accompaniedbyneuroinflammation.
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Synaptic dysfunction due to the disrupting binding of amyloid beta (Aβ) and tau oligomers is one of the earliest impairments in Alzheimer's Disease (AD), driving initial cognitive deficits and clinical manifestation.
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Basal forebrain cholinergic neurons (BFCNs) are believed to be one of the first cell types to be affected in all forms of AD, and their dysfunction is clinically correlated with impaired short-term memory formation and retrieval.
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Choline is an essential nutrient for humans.
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Alzheimer's disease (AD) is characterized by severe neuronal loss; however, the mechanisms by which neurons die remain elusive.
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High levels of amyloid-β peptide (Aβ) have been related to Alzheimer's disease pathogenesis.
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Morphological changes of dendritic spines are strongly associated with synaptic development and synaptic plasticity, which underlies learning and memory.
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The aim of this study was to investigate the effects of netrin-1 (NT-1) on amyloid-beta (Aβ)-induced impairments in learning-memory and synaptic plasticity.
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Alterations of the dopaminergic (DAergic) system are frequently reported in Alzheimer's disease (AD) patients and are commonly linked to cognitive and non-cognitive symptoms.
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The pathological potential of human astroglia in Alzheimer's disease (AD) was analysed in vitro using induced pluripotent stem cell (iPSC) technology.
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Activity-dependent synaptic plasticity phenomena such as long-term potentiation and long-term depression are candidate mechanisms for storing information in the brain.
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Astrocytes are key active elements of the brain that contribute to information processing.
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Cholinergic dysfunction has been associated with cognitive abnormalities in a variety of neurodegenerative and neuropsychiatric diseases.
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Tunicamycin (TM) induces endoplasmic reticulum (ER) stress and inhibits N-glycosylation in cells.
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This article updates the Calcium Hypothesis of Alzheimer's disease and brain aging on the basis of emerging evidence since 1994 (The present article, with the subtitle "New evidence for a central role of Ca 2+ in neurodegeneration," includes three appendices that provide context and further explanations for the rationale for the revisions in the updated hypothesis-the three appendices are as follows: Appendix I "Emerging concepts on potential pathogenic roles of [Ca 2+ ]," Appendix II "Future studies to validate the central role of dysregulated [Ca 2+ ] in neurodegeneration," and Appendix III "Epilogue: towards a comprehensive hypothesis.")
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Alzheimer's disease (AD) is a neurodegenerative disorder accompanied by severe progressive memory and cognitive impairment.
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Excitatory glutamatergic neurotransmission via N-methyl-d-aspartate receptor (NMDAR) is critical for synaptic plasticity and survival of neurons.
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Cell adhesion molecules (CAMs) have a pivotal role in building and maintaining synaptic structures during brain development participating in axonal elongation and pathfinding, glial guidance of neuronal migration, as well as myelination.
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Changes in gamma oscillations (20-50 Hz) have been observed in several neurological disorders.
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Perineuronal nets (PNNs) are unique extracellular matrix structures that wrap around certain neurons in the CNS during development and control plasticity in the adult CNS.
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Multiple cellular changes have been identified as being involved in Alzheimer's disease (AD) pathogenesis, including mitochondrial damage, synaptic loss, amyloid beta (Aβ) production and/or accumulation, inflammatory responses, and phosphorylated tau formation and/or accumulation.
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Ginkgo leaf is the most used form of supplement for cognitive ailments.
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39/100
Synaptic dysfunction has been recognized as an early feature occurring at the onset of Alzheimer's disease (AD).
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Chemical synapses are the predominant neuron-to-neuron contact in the central nervous system.
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Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive memory decline and subsequent loss of broader cognitive functions.
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N-methyl-D-aspartate receptors (NMDARs) play a pivotal role in the synaptic transmission and synaptic plasticity thought to underlie learning and memory.
From across this tag
9 of the 288 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 9. The same 9 appear here every time.
- Age-related cognitive deficits, impaired long-term potentiation and reduction in synaptic marker density in mice lacking the beta-amyloid precursor protein
- Suppression of eIF2α kinases alleviates Alzheimer's disease-related plasticity and memory deficits
- GFAP mRNA increases with age in rat and human brain
- APP processing and synaptic function
- Picomolar amyloid-beta positively modulates synaptic plasticity and memory in hippocampus
- Soluble Aβ oligomers inhibit long-term potentiation through a mechanism involving excessive activation of extrasynaptic NR2B-containing NMDA receptors
- Extrasynaptic NMDA receptor involvement in central nervous system disorders
- Neuronal cell killing by the envelope protein of HIV and its prevention by vasoactive intestinal peptide
- HIV secreted protein Tat prevents long-term potentiation in the hippocampal CA1 region