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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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Alzheimer's disease (AD) is an irreversible brain disorder characterized by progressive cognitive decline and neurodegeneration of brain regions that are crucial for learning and memory.
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Transgenic Tg2576 mice overexpressing human amyloid precursor protein (hAPP) are a widely used Alzheimer's disease (AD) mouse model to evaluate treatment effects on amyloid beta (Aβ) pathology and cognition.
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Alzheimer's disease (AD) is associated with defects of synaptic connectivity.
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Sharp wave ripples (SPW-Rs) represent the most synchronous population pattern in the mammalian brain.
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The extracellular matrix (ECM) is a critical regulator of neural network development and plasticity.
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In mature neurons, the number of synapses is determined by a neuronal activity-dependent dynamic equilibrium between positive and negative regulatory factors.
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Cognitive decline and disease progression in different neurodegenerative diseases typically involves synaptic dysfunction preceding the neuronal loss.
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36/100
Alzheimer's disease (AD) is the most common form of dementia in individuals over 65 years of age and is characterized by accumulation of beta-amyloid (Aβ) and tau.
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Alzheimer's disease (AD) is a devastating disease characterized by synaptic and neuronal loss in the elderly.
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Dose-dependent decrease of Aβ40 levels in vivo confirmed suppression of BACE1 activity by both inhibitors.
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All synapses are not the same. They differ in their morphology, molecular constituents, and malleability.
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In Alzheimer's disease (AD), memory impairment is the most prominent feature that afflicts patients and their families.
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Lithium is a well-established therapeutic option for the acute and long-term management of bipolar disorder and major depression.
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NMDA receptor (NMDAR)-induced excitotoxicity is thought to contribute to the cell death associated with certain neurodegenerative diseases, stroke, epilepsy, and traumatic brain injury.
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Environmental enrichment (EE) increases levels of novelty and complexity, inducing enhanced sensory, cognitive and motor stimulation.
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An early substantial loss of basal forebrain cholinergic neurons (BFCNs) is a constant feature of Alzheimer's disease (AD) and is associated with deficits in spatial learning and memory.
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Among all neurotrophins, brain-derived neurotrophic factor (BDNF) stands out for its high level of expression in the brain and its potent effects on synapses.
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Synapse loss and synaptic dysfunction are pathological processes already involved in the early stages of Alzheimer's disease (AD).
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Loss of neurons after brain injury and in neurodegenerative disease is often accompanied by reactive gliosis and scarring, which are difficult to reverse with existing treatment approaches.
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Age-related cognitive decline is accompanied by an increase of neuronal apoptosis and a dysregulation of neuroplasticity-related molecules such as brain-derived neurotrophic factor and neurotoxic factors including beta amyloid (Aβ) peptide.
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Soluble amyloid-β oligomers (Aβo) trigger Alzheimer's disease (AD) pathophysiology and bind with high affinity to cellular prion protein (PrP(C)).
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43/100
Expression of long-lasting synaptic plasticity and long-term memory requires protein synthesis, which can be repressed by phosphorylation of eukaryotic initiation factor 2 α-subunit (eIF2α).
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Impairment of cognitive processes is a devastating outcome of many diseases, injuries, and drugs affecting the central nervous system (CNS).
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36/100
Synaptic loss is the cardinal feature linking neuropathology to cognitive decline in Alzheimer's disease (AD).
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Extensive neuropathological studies have established a compelling link between abnormalities in structure and function of subcortical monoaminergic (MA-ergic) systems and the pathophysiology of Alzheimer's disease (AD).
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We show that a natural behavior, exploration of a novel environment, causes DNA double-strand breaks (DSBs) in neurons of young adult wild-type mice.
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Neurotoxic effects of amyloid β peptides are mediated through deregulation of intracellular Ca(2+) homeostasis and signaling, but relatively little is known about amyloid β modulation of Ca(2+) homeostasis and its pathological influence on glia.
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Glial cell-derived neurotrophic factor (GDNF), and the neurotrophin nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) are important for the survival, maintenance and regeneration of specific neuronal populations in the adult brain.
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The physiological role of the neurotrophin nerve growth factor (NGF) has been characterized, since its discovery in the 1950s, first in the sensory and autonomic nervous system, then in central nervous, endocrine and immune systems.
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β-amyloid (Aβ) is widely accepted to be one of the major pathomechanisms underlying Alzheimer's disease (AD), although there is presently lively debate regarding the relative roles of particular species/forms of this peptide.
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In light of the rising prevalence of Alzheimer's disease (AD), new strategies to prevent, halt, and reverse this condition are needed urgently.
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43/100
Amyloid-beta (Aβ) oligomers are thought to trigger Alzheimer's disease pathophysiology.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by the loss of cognitive functions, reflecting pathological damage to the medial prefrontal cortex (mPFC) as well as to the hippocampus and the entorhinal cortex.
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38/100
Neuronal calcium sensors (NCS) readily bind calcium and undergo conformational changes enabling them to interact and regulate specific target molecules.
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Neuroglial cells define brain homeostasis and mount defense against pathological insults.
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The EC (entorhinal cortex) is fundamental for cognitive and mnesic functions.
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The hippocampal formation has been implicated in a growing number of disorders, from Alzheimer's disease and cognitive ageing to schizophrenia and depression.
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Purinergic neurotransmission, involving release of ATP as an efferent neurotransmitter was first proposed in 1972.
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Aggregation of amyloid-β (Aβ) as toxic oligomers and amyloid plaques within the brain appears to be the pathogenic event that initiates Alzheimer's disease (AD) lesions.
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In Alzheimer's disease (AD), dementia severity correlates strongly with decreased synapse density in hippocampus and cortex.
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The mechanisms involved in Alzheimer's disease are not completely understood and how glial cells contribute to this neurodegenerative disease remains to be elucidated.
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Substantial progress has been made toward understanding the genetic architecture, cellular substrates, brain circuits and endophenotypic profiles of neuropsychiatric disorders, including autism spectrum disorders (ASD), schizophrenia and Alzheimer's disease.
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Amyloid beta (Aβ) oligomers accumulate in the brain tissue of Alzheimer disease patients and are related to disease pathogenesis.
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Glutamate transporters regulate normal synaptic network interactions and prevent neurotoxicity by rapidly clearing extracellular glutamate.
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The interaction between gene and environment is known to play a major role in the etiology of several neuropsychiatric disorders, including Alzheimer's disease (AD).
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In this mini-review/opinion article we describe evidence that multiple cellular and molecular alterations in Alzheimer's disease (AD) pathogenesis involve perturbed cellular calcium regulation, and that alterations in synaptic calcium handling may be early and pivotal events in the disease process.
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Lithium has been used clinically to treat bipolar disorder for over half a century, and remains a fundamental pharmacological therapy for patients with this illness.
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36/100
Planar microelectrode arrays (MEAs) are devices that can be used in biomedical and basic in vitro research to provide extracellular electrophysiological information about biological systems at high spatial and temporal resolution.
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Alzheimer's disease is the most frequent neurodegenerative disorder and the most common cause of dementia in the elderly.
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Disruption of axonal transport is a hallmark of several neurodegenerative diseases, including Alzheimer's disease (AD).
From across this tag
7 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 7. The same 7 appear here every time.
- Impaired Parahippocampal Gyrus-Orbitofrontal Cortex Circuit Associated with Visuospatial Memory Deficit as a Potential Biomarker and Interventional Approach for Alzheimer Disease
- Spinosin Attenuates Alzheimer's Disease-Associated Synaptic Dysfunction via Regulation of Plasmin Activity
- CRISPR/Cas9-Correctable mutation-related molecular and physiological phenotypes in iPSC-derived Alzheimer's PSEN2 N141I neurons
- Astrocytic ablation of truncated TrkB receptors reduces amyloid plaques and prevents synaptic loss in 5xFAD mice
- Long-term potentiation in the hippocampus: From magnesium to memory
- Benzothiazole amphiphiles promote RasGRF1-associated dendritic spine formation in human stem cell-derived neurons
- LIM-Kinases in Synaptic Plasticity, Memory, and Brain Diseases