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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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36/100
Brain-derived neurotrophic factor (BDNF) and serotonin (5-hydroxytryptamine, 5-HT) are known to regulate synaptic plasticity, neurogenesis and neuronal survival in the adult brain.
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Acutely developing lesions of the brain have been highly instructive in elucidating the neural systems underlying memory in humans and animal models.
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Learning and memory depend on dendritic spine actin assembly and docosahexaenoic acid (DHA), an essential n-3 (omega-3) polyunsaturated fatty acid (PFA).
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HIV-associated dementia (HAD) is a complication of advanced HIV disease.
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Glycogen synthase kinase3 (GSK3) is emerging as a prominent drug target in the CNS.
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Lithium is one of the most widely used mood-stabilizing agents for the treatment of bipolar disorder.
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Mutations in presenilins are the major cause of familial Alzheimer's disease, but the pathogenic mechanism by which presenilin mutations cause memory loss and neurodegeneration remains unclear.
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36/100
The ensuing homeostatic responses to myelin breakdown further increase intracortical toxicity and results in the relentless progression and non-random anatomical distribution of AD lesions that eventually cause neuronal dysfunction and degeneration.
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A large body of evidence has implicated Abeta peptides and other derivatives of the amyloid precursor protein (APP) as central to the pathogenesis of Alzheimer's disease (AD).
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder, which is probably caused by the cytotoxic effect of the amyloid beta-peptide (Abeta).
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Progressive neuronal loss and cognitive decline in Alzheimer's disease (AD) might be aggravated by beta-amyloid-enhanced excitotoxicity.
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Changes in hippocampal function seem critical for cognitive impairment in Alzheimer's disease (AD).
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Altered dendritic spines are characteristic of traumatized or diseased brain.
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Besides affecting the hypothalamus and other brain areas related to reproduction, ovarian steroids have widespread effects throughout the brain, on serotonin pathways, catecholaminergic neurons, and the basal forebrain cholinergic system as well as the hippocampal formation, a brain region involved in spatial and declarative memory.
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The dementia in Alzheimer disease (AD) is usually attributed to widespread neuronal loss in conjunction with the pathologic hallmarks of intracellular neurofibrillary tangles and extracellular plaques containing amyloid (A beta) in fibrillar form.
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Besides their well-established actions on reproductive functions, estrogens exert a variety of actions on many regions of the nervous system that influence higher cognitive function, pain mechanisms, fine motor skills, mood, and susceptibility to seizures; they also appear to have neuroprotective actions in relation to stroke damage and Alzheimer's disease.
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Glycogen synthase kinase-3beta (GSK3beta) is a fascinating enzyme with an astoundingly diverse number of actions in intracellular signaling systems.
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36/100
Brain tissue has a remarkable ability to accumulate glutamate.
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Alzheimer's Disease (AD) is the most common of the senile dementias, the prevalence of which is increasing rapidly, with a projected 14 million affected worldwide by 2025.
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40/100
The expression levels of three synaptic proteins (synaptophysin, synaptotagmin, and growth-associated protein 43 [GAP43]) in AD cases clinically classified by Clinical Dementia Rating (CDR) score were analyzed.
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HIV-associated dementia complex is a serious disabling disease characterized by cognitive, behavioral and motor dysfunction.
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Besides its fast excitatory properties, glutamate is known to have neurotoxic properties when released in large amounts or when incompletely recycled.
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36/100
Physical activity and antidepressant treatment have each separately been of significant interest for the management of Alzheimer's disease (AD); particularly the behavioral problems associated with this dementing disorder.
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Neuronal degeneration in Alzheimer's disease (AD) has been variously attributed to increases in cytosolic calcium, reactive oxygen species, and phosphorylated forms of the microtubule-associated protein tau. beta-Amyloid (betaA), which accumulates extracellularly in AD brain, induces calcium influx in culture via the L voltage-sensitive calcium channel.
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Recent advances in cellular and molecular biology have resulted in the identification of two novel, hitherto completely unexpected targets of lithium's actions, discoveries that may have a major impact on the future use of this unique cation in biology and medicine.
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Mutations in the beta-amyloid precursor protein are strongly associated with some cases of familial Alzheimer's disease.
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41/100
The mammalian brain has a high degree of plasticity, with dentate granule cell neurogenesis and glial proliferation stimulated by an enriched environment combining both complex inanimate and social stimulation.
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The vulnerability of neurons and the irreversibility of loss make discoveries of neuroprotective compounds fundamentally important.
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We investigated synaptic communication and plasticity in hippocampal slices from mice overexpressing mutated 695-amino-acid human amyloid precursor protein (APP695SWE), which show behavioral and histopathological abnormalities simulating Alzheimer's disease.
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Transcription factors provide the link between early membrane-proximal signalling events and changes in gene expression.
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The mechanisms of synapse damage in Alzheimer's disease (AD) are not fully understood.
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Nicotine obtained from tobacco can improve learning and memory on various tasks and has been linked to arousal, attention, rapid information processing, working memory, and long-term memories that can cause craving years after someone has stopped smoking.
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A novel 14-amino acid peptide, with stress-protein-like sequences, exhibiting neuroprotection at unprecedented concentrations, is revealed.
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Recent findings link altered processing of beta-amyloid precursor protein (beta APP) to disruption of neuronal Ca2+ homeostasis and an excitotoxic mechanism of cell death in Alzheimer's disease.
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Glial fibrillary acidic protein (GFAP) mRNA was examined by RNA blot hybridization in three age groups of two cohorts of male F-344 rats and in 47 human postmortem brain samples.
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Brain cholinergic neurons are critical for memory function and their loss may contribute to memory impairment in Alzheimer's disease.
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The clinical manifestations of AIDS (acquired immune deficiency syndrome) often include neuropsychiatric and neurological deficits, including early memory loss and progressive dementia.
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In Alzheimer's disease, the relatively selective depression of neocortical cholinergic innervation may be closely associated with the neuronal loss in Ch4, which has also been described inthis condition.
From across this tag
8 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 8. The same 8 appear here every time.
- Abeta oligomer-induced aberrations in synapse composition, shape, and density provide a molecular basis for loss of connectivity in Alzheimer's disease
- The Role of ADF/Cofilin in Synaptic Physiology and Alzheimer's Disease
- LATS2 modulates synaptic organization and function by regulating actin dynamics
- Cholesterol imbalance and neurotransmission defects in neurodegeneration
- Group 1 mGluR-dependent synaptic long-term depression: mechanisms and implications for circuitry and disease
- Role of phosphodiesterases in the pathophysiology of neurodevelopmental disorders
- Synaptic Plasticity and Memory: New Insights from Hippocampal Left-Right Asymmetries
- SNCA genetic lowering reveals differential cognitive function of alpha-synuclein dependent on sex