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transgenic
1,157 studies tagged transgenic, dated 1986-01-01 to 2026-09-25. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- What Do Sugar, Gila Monsters, and the Therapeutic Dance Have in Common With GLP-1RA, Stroke, and Dementia? 2026-09-25
- Myo-inositol as a spectroscopic marker of neuroinflammation in frontotemporal lobar degeneration 2026-09-20
- Laromestrocel preserves brain volume and cognitive function in Alzheimers disease by inhibiting neuroinflammation 2026-09-17
Studies
1,157 studies carry this tag.
Date range
1986 to 2026
Top journals
- The Journal of biological chemistry 109
- The Journal of neuroscience : the official journal of the Society for Neuroscience 42
- Proceedings of the National Academy of Sciences of the United States of America 39
- Neuron 28
- Nature 23
363 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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Amyloid plaques are a neuropathological hallmark of Alzheimer's disease (AD), but their relationship to neurodegeneration and dementia remains controversial.
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A study on long-term astrocytic responses (from 1 day to 20 months after lesioning in 4-month-old rats, and from 1 day to 6 months in 20-month-old rats) to diverse unilateral damage of the nucleus basalis (nbM) by injection of 40 nmol of ibotenic acid, or 50 or 100 nmols of quisqualic acid was performed using a histochemical method (immunoreactivity against the glial fibrillary acidic protein GFAP).
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Previous studies have demonstrated that amyloid precursor protein (APP) can bind and reduce Cu(II) to Cu(I), leading to oxidative modification of APP.
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The numbers of immune-activated brain mononuclear phagocytes (MPs) affect the progression of human immunodeficiency virus (HIV)-1-associated dementia (HAD).
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The mechanisms responsible for the pathological deposition of brain iron in Parkinson's disease, Alzheimer's disease and other human neurodegenerative disorders remain poorly understood.
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AIDS dementia is characterized by neuronal loss in association with synaptic damage.
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HIV-1 glycoprotein gp120 induces injury and apoptosis in rodent and human neurons in vitro and in vivo and is therefore thought to contribute to HIV-associated dementia.
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The cholinergic system is one of the most important modulatory neurotransmitter systems in the brain and controls activities that depend on selective attention, which are an essential component of conscious awareness.
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Receptor for advanced glycation end products (RAGE) is a member of the immunoglobulin superfamily of cell surface molecules and engages diverse ligands relevant to distinct pathological processes.
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Alzheimer's disease (AD) is the commonest form of adult onset dementia and is characterised neuropathologically by the accumulation of plaques containing beta-amyloid (A beta) fibrils, reactive astrocytes, activated microglia, and leukocytes.
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Microglia are the main human immunodeficiency virus (HIV) reservoir in the central nervous system and most likely play a major role in the development of HIV dementia (HIVD).
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Neurofibrillary tangles (NFTs) form in a number of neurodegenerative disorders.
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48/100
The presynaptic protein alpha-synuclein has been implicated in the pathogenesis of Parkinson's disease.
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[3H]inositol(1,4,5)-trisphosphate (IP3) binding studies have shown decreased [3H]IP3 binding to brain tissue in several neurodegenerative diseases, including Alzheimer's and Huntington's diseases.
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The presenilin (PS) genes associated with Alzheimer disease encode polytopic transmembrane proteins which undergo physiologic endoproteolytic cleavage to generate stable NH2- and COOH-terminal fragments (NTF or CTF) which co-localize in intracellular membranes, but are tightly regulated in their stoichiometry and abundance.
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The amyloid precursor protein (APP) plays a crucial role in the pathogenesis of Alzheimer's disease.
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56/100
Abeta1-42 is a self-associating peptide whose neurotoxic derivatives are thought to play a role in Alzheimer's pathogenesis.
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We recently identified a cDNA encoding a human brain specific trypsinogen (trypsinogen IV).
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Microglia-mediated inflammatory responses have been implicated in the pathogenesis of neuritic plaques in Alzheimer's disease.
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The neural protein FE65 contains two types of protein-protein interaction modules: one WW binding domain and two phosphotyrosine binding domains.
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Entry of the type 1 human immunodeficiency virus into most cells requires the presence of the CD4 protein in combination with one of several recently described co-receptors.
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Among the 30 boxers, 11 were found to be normal (CBI score=0), 12 showed mild deficits (CBI score=1-2), 4 were moderately impaired (CBI score=3-4), and 3 showed signs of severe impairment (CBI score > 4).
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The pathogenesis of HIV-associated cognitive changes is poorly understood.
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47/100
Alzheimer's disease (AD) is a devastating neurological disorder characterized by loss of cognitive skills and progressive dementia.
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Several members of the chemokine receptor family are used together with CD4 for HIV-1 entry into target cells.
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The molecular basis for the degeneration of neurons and the deposition of amyloid in plaques and in the cerebrovasculature in Alzheimer's disease (AD) is incompletely understood.
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Stroke is the third leading cause of death, and vascular dementia the second cause of dementia after Alzheimer's disease.
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In patients with dementia, a positive immunoassay for the 14-3-3 brain protein in cerebrospinal fluid strongly supports a diagnosis of Creutzfeldt-Jakob disease.
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The majority of HIV-1-infected individuals manifest a plethora of central nervous system (CNS) diseases unrelated to opportunistic infections, including AIDS dementia complex, encephalitis, and various other disorders of the CNS.
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Human immunodeficiency virus (HIV) infection is commonly associated with neurological disease that occurs in the apparent absence of extensive infection of brain cells by HIV, suggesting that indirect mechanisms account for neuropathogenesis in the CNS, perhaps including changes in the normal neuroprotective functions of astrocytes.
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32/100
B/A4 is the major component of brain amyloid plaque, one of the hallmarks of Alzheimer's disease (AD).
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The very low density lipoprotein receptor (VLDL-r) is a cell-surface molecule specialized for the internalization of multiple diverse ligands, including apolipoprotein E (apoE)-containing lipoprotein particles, via clathrin-coated pits.
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Mutations in the human Cu,Zn superoxide dismutase gene (SOD1) are found in 20% of kindreds with familial amyotrophic lateral sclerosis.
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Transgenic mice expressing the oncogenic protein-serine/threonine kinase Mos at high levels in the brain display progressive neuronal degeneration and gliosis.
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As in Alzheimer-disease (AD) brain, vacuolated muscle fibers of inclusion-body myositis (IBM) contain abnormally accumulated beta-amyloid precursor protein (beta APP), including its beta-amyloid protein epitope, and increased beta APP-751 mRNA.
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Possible roles of the complement (C) system in the normal and injured brain were explored with inbred mice that carried a frameshift mutation in the C5 gene.
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Two chemokine (chemoattractant cytokines) beta peptides, macrophage inflammatory proteins 1 alpha and 1 beta (MIP-1 alpha and MIP-1 beta), were induced in human monocyte cultures following infection with the human immunodeficiency virus type 1 (HIV-1).
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S100 beta protein, a member of a Ca(2+)-binding protein family present primarily in the nervous system, affects the survival and differentiation of both neurons and glia cells.
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Neurodegenerative processes in Alzheimer disease (AD) are thought to be driven in part by the deposition of amyloid beta (A beta), a 39- to 43-amino acid peptide product resulting from an alternative cleavage of amyloid precursor protein.
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The epsilon 4 allele of apolipoprotein E (apoE) is a major risk factor for Alzheimer disease, suggesting that apoE may directly influence neurons in the aging brain.
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Formalin-fixed postmortem brain tissue from 14 HIV-infected adult patients, with previous repeated neurological and neuroradiological examinations, was studied by immunohistochemical and molecular biological methods.
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Stimulation of muscarinic m1 or m3 receptors can, by generating diacylglycerol and activating protein kinase C, accelerate the breakdown of the amyloid precursor protein (APP) to form soluble, nonamyloidogenic derivatives (APPs), as previously shown.
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Senile plaques found in the brains of patients with Alzheimer's disease (AD) are surrounded by clusters of reactive microglia.
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We studied a synatophysin-like immunoreactivity in the hippocampal formation of patients with definite Alzheimer's disease, multi-infarct dementia, patients with no evidence of clinical dementia with neuropathological findings fulfilling the criteria of possible Alzheimer's disease, and age-matched nondemented controls.
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Biological effects related to cell growth, as well as a role in the pathogenesis of Alzheimer disease, have been ascribed to the beta-amyloid precursor protein (beta-APP).
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The beta-amyloid or beta/A4 peptides that accumulate as filamentous aggregates in the extracellular space of Alzheimer disease (AD) brains are derived from one or more alternatively spliced amyloid precursor proteins (APPs).
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The metabolic fate of the Alzheimer beta/A4 amyloid precursor protein (APP) includes intraamyloid proteolysis that leads to the production of secreted N-terminal and cell-associated C-terminal fragments.
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Kainic acid lesions of rat striatum caused an elevation of amyloid precursor protein (APP) immunoreactivity in neurons and neurites, some of which were then phagocytosed by reactive microglia/macrophages.
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Antibodies to ubiquitin have been used to search for evidence of abnormal protein degradation in amyotrophic lateral sclerosis--motor neuron disease (ALS).
From across this tag
10 of the 1,153 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 10. The same 10 appear here every time.
- Astrocyte glypican 5 regulates synapse maturation and stabilization
- Reduction of Neuroinflammation as a Common Mechanism of Action of Anorexigenic and Orexigenic Peptide Analogues in the Triple Transgenic Mouse Model of Alzheimer´s Disease
- Neurotoxicity of advanced glycation end-products for cultured cortical neurons
- Contribution of presenilin transmembrane domains 6 and 7 to a water-containing cavity in the gamma-secretase complex
- Phenolic compounds prevent amyloid β-protein oligomerization and synaptic dysfunction by site-specific binding
- Apolipoprotein E4 impairs the response of neurodegenerative retinal microglia and prevents neuronal loss in glaucoma
- Astrocytes upregulate interleukin-15 in response to neuroinflammation during Alzheimer's disease
- AGEs/RAGE complex upregulates BACE1 via NF-κB pathway activation
- Therapeutic Effects of Transplanted Exosomes Containing miR-29b to a Rat Model of Alzheimer's Disease
- Increases of SET level and translocation are correlated with tau hyperphosphorylation at ser202/thr205 in CA1 of Ts65Dn mice