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plasticity
287 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
287 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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The precise mechanisms that lead to cognitive decline in Alzheimer's disease are unknown.
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41/100
Alzheimer's disease (AD) is the main cause of dementia worldwide.
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These results suggest that the targeted methylation of APP via dCas9-Dnmt3a treatment can be a potential therapeutic strategy for AD.
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Recently, we found that all proteins required for necroptosis execution, a previously defined programmed form of neuronal cell death, are present in GVD, such as the phosphorylated necroptosis executioner mixed-lineage kinase domain-like protein (pMLKL).
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45/100
Synaptic dysfunction is an early mechanism in Alzheimer's disease that involves progressively larger areas of the brain over time.
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Synaptic dysfunction is closely related to Alzheimer's disease (AD) which is also recognized as synaptic disorder. β-amyloid (Aβ) is one of the main pathogenic factors in AD, which disrupts synaptic plasticity and mediates the synaptic toxicity through different mechanisms.
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Alzheimer's disease (AD) is a neurodegenerative disease characterized by the progressive deterioration of cognitive functions.
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41/100
Trans-anethole is an aromatic compound that has been studied for its anti-inflammation, anticonvulsant, antinociceptive, and anticancer effects.
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Lateral ventricle administration, but not caudal vein injection of BMSC-exos improved AD-like behaviors in the STZ-injected mouse model, as indicated by the increased number of rearing, increased frequency to the central area, and increased duration and distance traveled in the central area in the OFT, and improved preference index of the novel object in the NOR.
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Hippocampus is the significant component of the limbic lobe, which is further subdivided into the dentate gyrus and parts of Cornu Ammonis.
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Synaptic abnormalities are a cardinal feature of Alzheimer's disease (AD) that are known to arise as the disease progresses.
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Calcium/calmodulin-dependent protein kinase II (CaMKII) and neuronal store-operated calcium entry (nSOCE) have been implicated in the development of Alzheimer's disease (AD). nSOCE is involved in regulation of dendritic spine shape, particularly in stability of mushroom spines that play role in formation of strong synapses.
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Long-lasting changes of synaptic efficacy are largely mediated by activity-induced gene transcription and are essential for neuronal plasticity and memory.
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Impairments in activities of daily living (ADL) are common clinical symptoms of human Alzheimer's disease (AD).
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TDP-43 proteinopathy is linked to neurodegenerative diseases that feature synaptic loss in the cortex and hippocampus, although it remains unclear how TDP-43 regulates mature synapses.
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Memory impairments are associated with many brain disorders such as autism, Alzheimer's disease, and depression.
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The CSF level of Ng was significantly higher, whereas the NPTXR was significantly lower in the AD patients than in cognitively healthy controls.
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Learning and memory require structural and functional modifications of synaptic connections, and synaptic deficits are believed to underlie many brain disorders.
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Alzheimer's disease (AD) is a progressive neurodegenerative disease with no cure.
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The ability to investigate therapeutic interventions in animal models of neurodegenerative diseases depends on extensive characterization of the model(s) being used.
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The data revealed that 5XFAD mice that received hMSC-EV treatment behaved significantly better in cognitive tests than saline treated 5XFAD mice, with no significant change between EV-treated 5XFAD mice and NT mice.
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Brain plasticity is widely accepted as the core neurophysiological basis of memory and is generally defined by activity-dependent changes in synaptic efficacy, such as long-term potentiation (LTP) and long-term depression (LTD).
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Astrocytes, through their numerous processes, establish a bidirectional communication with neurons that is crucial to regulate synaptic plasticity, the purported neurophysiological basis of memory.
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The vascular endothelial growth factor (VEGF) pathway regulates key processes in synapse function, which are disrupted in early stages of Alzheimer's disease (AD) by toxic-soluble amyloid-beta oligomers (Aβo).
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The prefrontal cortex (PFC) serves as the chief executive officer of the brain, controlling the highest level cognitive and emotional processes.
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Dopamine (DA) is a key neurotransmitter involved in multiple physiological functions including motor control, modulation of affective and emotional states, reward mechanisms, reinforcement of behavior, and selected higher cognitive functions.
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Cognitive reserve is originally an epidemiological concept that encompasses individual abilities to cope with changes.
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41/100
Alterations in brain cholesterol homeostasis in midlife are correlated with a higher risk of developing Alzheimer's disease (AD).
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In this review, we focus on the potential role of the γ-aminobutyric acidergic (GABAergic) system in age-related episodic memory impairments in humans, with a particular focus on Alzheimer's disease (AD).
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Beta-amyloid (Aβ) has been recognized as an early trigger in the pathogenesis of Alzheimer's disease (AD) leading to synaptic and cognitive impairments.
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Chronic cerebral hypoperfusion (CCH) may lead to the cognitive dysfunction, but the underlying mechanisms are unclear.
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We identify Clu as an astrocyte-derived synaptogenic and anti-amyloid factor; the combination of these activities may influence the progression of late-onset AD.
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Phosphodiesterases (PDEs) are enzymes involved in the homeostasis of both cAMP and cGMP.
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The expression of ABCA1 was significantly downregulated in AD models at both mRNA and protein levels.
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P021 treatment during early development prevented cognitive impairment and increased expressions of pCREB and BDNF that activated downstream various signaling cascades such as PLC/PKC, MEK/ERK and PI3K/Akt, and ameliorated synaptic protein deficit in 4-month-old 3xTg-AD mice.
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Alzheimer's disease (AD) is a neurodegenerative disease characterized by neurological dysfunction, including memory impairment, attributed to the accumulation of amyloid β (Aβ) in the brain.
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The synaptic regulator, kalirin, plays a key role in synaptic plasticity and formation of dendritic arbors and spines.
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Actin-depolymerization factor (ADF)/cofilin, a family of actin-binding proteins, are critical for the regulation of actin reorganization in response to various signals.
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41/100
Protein prenylation is a post-translational lipid modification that governs a variety of important cellular signaling pathways, including those regulating synaptic functions and cognition in the nervous system.
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Brain-derived neurotrophic factor (BDNF) is one of the most distributed and extensively studied neurotrophins in the mammalian brain.
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We found a beginning synaptic impairment (LTP deficit) at 3-4 months in the prefrontal cortex of AppNL-G-F mice that is further aggravated and extended to the hippocampus at 6-8 months.
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Alzheimer's disease (AD) is a neurodegenerative disorder characterized clinically by severe cognitive deficits and pathologically by amyloid plaques, neuronal loss, and neurofibrillary tangles.
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39/100
Synaptic plasticity is the neural basis of physiological processes involved in learning and memory.
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The hippocampus is important for memory formation and is severely affected in the brain with Alzheimer disease (AD).
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Dendrites and dendritic spines are dynamic structures with pivotal roles in brain connectivity and have been recognized as the locus of long-term synaptic plasticity related to cognitive processes such as learning and memory.
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The parahippocampal gyrus-orbitofrontal cortex (PHG-OFC) circuit in humans is homologous to the postrhinal cortex (POR)-ventral lateral orbitofrontal cortex (vlOFC) circuit in rodents.
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The strength and efficiency of synaptic connections are affected by the environment or the experience of the individual.
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Hippocampal synaptic dysfunction is a hallmark of Alzheimer's disease (AD).
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Synaptic dysfunction has been implicated as an early cause of cognitive decline in neurodegenerative diseases (NDDs) such as Alzheimer's disease (AD).
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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.
From across this tag
8 of the 287 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 8. The same 8 appear here every time.
- Deciphering the molecular basis of memory failure in Alzheimer's disease
- Long-term social isolation exacerbates the impairment of spatial working memory in APP/PS1 transgenic mice
- Targeting SUMO-1ylation Contrasts Synaptic Dysfunction in a Mouse Model of Alzheimer's Disease
- Riluzole reduces amyloid beta pathology, improves memory, and restores gene expression changes in a transgenic mouse model of early-onset Alzheimer's disease
- Astrocyte function from information processing to cognition and cognitive impairment
- The β-adrenergic hypothesis of synaptic and microglial impairment in Alzheimer's disease
- Casting a Wide Net: Role of Perineuronal Nets in Neural Plasticity
- A delicate balance: role of MMP-9 in brain development and pathophysiology of neurodevelopmental disorders