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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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Prenatal exposure to low doses of LPS caused AD-related features including behavioral and neuropathological changes from midlife to senectitude.
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ATP13A2 (PARK9) is a late endolysosomal transporter that is genetically implicated in a spectrum of neurodegenerative disorders, including Kufor-Rakeb syndrome-a parkinsonism with dementia 1 -and early-onset Parkinson's disease 2 .
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Quercetin is a polyphenol with multiple biological activities, and results of our preliminary study showed that it could shorten the immobility time of mice in the forced swimming test and tail suspending test.
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57/100
There are few validated fluid biomarkers in frontotemporal dementia (FTD).
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The AD set included 23,092 cases and 30,920 controls, the ALS set included 7391 cases and 12,442 controls, and the PD set included 8498 patients and 9161 controls.
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Neuroinflammation is a common feature shared by neurodegenerative disorders, such as Parkinson's disease (PD), and seems to play a key role in their development and progression.
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38/100
Mutations in the GBA1 gene are the most common genetic risk factor for Parkinson's disease (PD) and dementia with Lewy bodies (DLB).
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Pomegranate juice (PGJ) is rich in unique bioactive compounds that can be used in the management of various diseases/disorders such as cancer, heart disease, Alzheimer disease, hypertension, and diabetes.
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Activated Caspase-6 (Casp6) is associated with age-dependent cognitive impairment and Alzheimer disease (AD).
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A promising new therapeutic target for the treatment of Alzheimer's disease (AD) is the circadian system.
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Thalamic atrophy is a common feature across all forms of FTD but little is known about specific nuclei involvement.
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ApoE4 impairs pericyte-mediated basement membrane formation, potentially contributing to the cerebrovascular effects of apoE4.
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Noncoding small RNAs, such as microRNAs, are becoming the biomarkers of choice for multiple diseases in clinical diagnostics.
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Microglia mediate multiple facets of neuroinflammation, which plays a double-edged role in various brain diseases via distinct microglial phenotypes (deleterious M1 and neuroprotective M2).
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44/100
Insulin resistance associates with increased risk for cognitive decline and dementia; however, the underpinning mechanisms for this increased risk remain to be fully defined.
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With increased life expectancy worldwide, there is an urgent need for improving preventive measures that delay the development of age-related degenerative diseases.
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Alzheimer's disease (AD) is the most common dementia in the elderly.
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Alzheimer's disease is the most prevalent type of dementia and is caused by the deposition of extracellular amyloid-beta and abnormal tau phosphorylation.
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Microglia transform from homeostatic to disease-associated-microglia (DAM) profiles in neurodegeneration.
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Stress granules (SGs) form during cellular stress and are implicated in neurodegenerative diseases such as amyotrophic lateral sclerosis and frontotemporal dementia (ALS/FTD).
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The genetic variant rs72824905-G (minor allele) in the PLCG2 gene was previously associated with a reduced Alzheimer's disease risk (AD).
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41/100
The GGGGCC repeat expansion in C9ORF72 is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
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Neuronal and synaptic loss is characteristic in many neurodegenerative diseases, such as frontotemporal dementia and Alzheimer's disease.
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Microglia have important remodeling functions in neurodevelopment, aging, and disease, with evidence for molecular diversity.
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Cerebral amyloid angiopathy (CAA) results from amyloid-β deposition in the cerebrovasculature.
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Alzheimer disease has been well associated with mitochondrial dysfunctions.
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44/100
Imbalance in production and clearance of amyloid beta (Aβ) is the primary reason for its deposition in Alzheimer disease.
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Crocus sativus L. natural compounds have been extensively used in traditional medicine for thousands of years.
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Glial activation and neuroinflammation play significant roles in apoptosis as well as in the development of cognitive and memory deficits.
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Increasing evidences support the notion that the impairment of intracellular degradative machinery is responsible for the accumulation of oxidized/misfolded proteins that ultimately results in the deposition of protein aggregates.
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While cytoplasmic aggregation of TDP-43 is a pathological hallmark of amyotrophic lateral sclerosis and frontotemporal dementia, how aggregates form and what drives its nuclear clearance have not been determined.
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Signaling between the endoplasmic reticulum (ER) and mitochondria regulates a number of key neuronal functions.
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Microglia are the principal innate immune defense cells of the centeral nervous system (CNS) and the target of the human immunodeficiency virus type one (HIV-1).
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38/100
Tau inclusions are a shared feature of many neurodegenerative diseases, among them frontotemporal dementia caused by tau mutations.
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TDP-43 proteinopathy is a pathological hallmark of amyotrophic lateral sclerosis and frontotemporal dementia where cytoplasmic TDP-43 inclusions are observed within degenerating regions of patient postmortem tissue.
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50/100
Pathological aggregation of the transactive response DNA-binding protein of 43 kDa (TDP-43) is associated with several neurodegenerative disorders, including ALS, frontotemporal dementia, chronic traumatic encephalopathy, and Alzheimer's disease.
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Our in vivo model of c9FTD/ALS is the first to robustly recapitulate hallmark features derived from both sense and antisense C9orf72 repeat-associated transcripts complete with neurodegeneration and behavioral impairments.
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TAR DNA binding protein 43 (TDP-43) is a versatile RNA/DNA binding protein involved in RNA-related metabolism.
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Mutations in RNA-binding proteins (RBPs) localized in ribonucleoprotein (RNP) granules, such as hnRNP A1 and TDP-43, promote aberrant protein aggregation, which is a pathological hallmark of various neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
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It has been well documented that neurotrophins, including brain-derived neurotrophic factor (BDNF), are severely affected in Alzheimer's disease (AD), but their administration faces a myriad of technical challenges.
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Alzheimer's disease (AD) is a heterogeneous disorder with multiple etiologies.
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Type I interferons (IFN-I) are the principal antiviral molecules of the innate immune system and can be made by most cell types, including central nervous system cells.
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Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are associated with loss of nuclear transactive response DNA-binding protein 43 (TDP-43).
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Apoptosis is crucial for the normal development of the nervous system, whereas neurons in the adult CNS are relatively resistant to this form of cell death.
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Mutations in the microtubule-associated protein tau (MAPT) gene cause autosomal dominant frontotemporal lobar degeneration with tau inclusions (FTLD-tau).
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Triggering receptor expressed on myeloid cells-2 (TREM2) is an innate immune receptor that promotes phagocytosis by myeloid cells such as microglia and macrophages.
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Alzheimer disease (AD) is a complex pathology related to multiple causes including oxidative stress.
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The 751 study participants were older (median age [interquartile range], 87 years [51-105 years]), 395 (54%) were women, and 324 (44%) were APOE ε4 carriers.
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Through the generation of humanized FUS mice expressing full-length human FUS, we identify that when expressed at near endogenous murine FUS levels, both wild-type and ALS-causing and frontotemporal dementia (FTD)-causing mutations complement the essential function(s) of murine FUS.
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TYROBP/DAP12 forms complexes with ectodomains of immune receptors (TREM2, SIRPβ1, CR3) associated with Alzheimer's disease (AD) and is a network hub and driver in the complement subnetwork identified by multi-scale gene network studies of postmortem human AD brain.
From across this tag
9 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 9. The same 9 appear here every time.
- Expression profiles for macrophage alternative activation genes in AD and in mouse models of AD
- High-fidelity and differential nonsense suppression in live cells and a frontotemporal dementia allele with human transfer RNAs
- Cytoplasmic expression of trans-active response DNA-binding protein-43 in aged mice display hippocampal sclerosis-like degeneration and neuronal loss with reduced lifespan
- The polyphenol oleuropein aglycone protects TgCRND8 mice against Aß plaque pathology
- Chronic treatment with the gamma-secretase inhibitor LY-411,575 inhibits beta-amyloid peptide production and alters lymphopoiesis and intestinal cell differentiation
- Neuroanatomical distribution of CXCR4 in adult rat brain and its localization in cholinergic and dopaminergic neurons
- Analysis of the hippocampal proteome in ME7 prion disease reveals a predominant astrocytic signature and highlights the brain-restricted production of clusterin in chronic neurodegeneration
- Dantrolene ameliorates cognitive decline and neuropathology in Alzheimer triple transgenic mice
- TDP-43 mediates degeneration in a novel Drosophila model of disease caused by mutations in VCP/p97