Home › Research › Topics › mice
mice
1,163 studies tagged mice, 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
1,163 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
365 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.
-
DJ-1 is an oxidative stress sensor that localizes to the mitochondria when the cell is exposed to oxidative stress.
-
γ-Secretase generates amyloid β-protein (Aβ), a pathogenic molecule in Alzheimer disease, through the intramembrane cleavage of the β-carboxyl-terminal fragment (βCTF) of β-amyloid precursor protein.
-
Prion diseases are characterized by accumulation of misfolded protein, gliosis, synaptic dysfunction, and ultimately neuronal loss.
-
Alzheimer's disease (AD) is the most common type of dementia.
-
As a major characteristic of aging process, neuroinflammation is involved in the pathogenesis of several aging-related diseases including Alzheimer's disease (AD).
-
Reprogramming somatic cells to induced pluripotent stem cells (iPSCs) resets their identity back to an embryonic age and, thus, presents a significant hurdle for modeling late-onset disorders.
-
Alzheimer's disease (AD) is the most prevalent form of dementia in the elderly population.
-
Alzheimer's disease (AD) is the leading cause of dementia and has no cure.
-
Decline of cognition and increasing risk of neurodegenerative diseases are major problems associated with aging in humans.
-
The GGGGCC (G4C2) intronic repeat expansion within C9ORF72 is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
-
Basal forebrain cholinergic neurons play an important role in cognitive functions such as learning and memory, and they are affected in several neurodegenerative diseases, including Alzheimer disease and Down syndrome.
-
57/100
The finding that a GGGGCC (G4C2) hexanucleotide repeat expansion in the chromosome 9 ORF 72 (C9ORF72) gene is a common cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) links ALS/FTD to a large group of unstable microsatellite diseases.
-
Prions are proteins that adopt alternative conformations, which become self-propagating.
-
Expanded hexanucleotide repeats in the chromosome 9 open reading frame 72 (C9orf72) gene are the most common genetic cause of ALS and frontotemporal degeneration (FTD).
-
Massive GGGGCC repeat expansion in the first intron of the gene C9orf72 is the most common known cause of familial frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS).
-
Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are devastating neurodegenerative disorders with clinical, genetic, and neuropathological overlap.
-
Delayed neuronal loss and brain atrophy after cerebral ischemia contribute to stroke and dementia pathology, but the mechanisms are poorly understood.
-
54/100
Hexanucleotide repeat expansion in C9ORF72 is the most common genetic cause of frontotemporal dementia and motor neuron disease.
-
A hexanucleotide GGGGCC repeat expansion in the noncoding region of the C9ORF72 gene is the most common genetic abnormality in familial and sporadic amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
-
53/100
Amyotrophic lateral sclerosis (ALS) is a severe neurodegenerative condition characterized by loss of motor neurons in the brain and spinal cord.
-
Defects in DNA repair have been extensively linked to neurodegenerative diseases, but the exact mechanisms remain poorly understood.
-
As neuroinflammation is an early event in the pathogenesis of Alzheimer' s disease, new selective antiinflammatory drugs could lead to promising preventive strategies.
-
Systemic inflammatory events often precipitate acute cognitive dysfunction in elderly and demented populations.
-
Phagocytosis controls CNS homeostasis by facilitating the removal of unwanted cellular debris.
-
Alzheimer's disease (AD) involves several possible molecular mechanisms, including impaired brain insulin signaling and glucose metabolism.
-
DNAX-activating protein of 12 kD (DAP12) is an immunoreceptor tyrosine-based activation motif (ITAM)-containing adaptor protein found in myeloid cells and natural killer cells, and it couples to various receptors that mediate either cellular activation or inhibition.
-
The claimed beneficial effects of the Mediterranean diet include prevention of several age-related dysfunctions including neurodegenerative diseases and Alzheimer-like pathology.
-
Breakthrough discoveries identifying common genetic causes for amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) have transformed our view of these disorders.
-
TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00257712.
-
Excessive proteolytic breakdown of the amyloid precursor protein (APP) to neurotoxic amyloid β peptides (Aβ) by secretases in the brain is a molecular cause of Alzheimer disease (AD).
-
Alzheimer's disease (AD) is the most common type of age-related dementia.
-
Stress granules and P bodies are conserved cytoplasmic aggregates of nontranslating messenger ribonucleoprotein complexes (mRNPs) implicated in the regulation of mRNA translation and decay and are related to RNP granules in embryos, neurons, and pathological inclusions in some degenerative diseases.
-
Schizophrenia is characterized by reduced hippocampal volume, decreased dendritic spine density, altered neuroplasticity signaling pathways, and cognitive deficits associated with impaired hippocampal function.
-
PICALM, a clathrin adaptor protein, plays important roles in clathrin-mediated endocytosis in all cell types.
-
Recent evidence suggests that rare genetic variants within the TREM2 gene are associated with increased risk of Alzheimer's disease.
-
Quinolinic acid is a product of tryptophan degradation and may serve as a precursor for NAD(+), an important enzymatic cofactor for enzymes such as the DNA repair protein PARP.
-
Accumulation of β-amyloid (Aβ) in the brain is a key event in Alzheimer disease pathogenesis.
-
Alzheimer disease (AD) brain is characterized by extracellular plaques of amyloid β (Aβ) peptide with reactive microglia.
-
The normal on and off switching of the PI3-K (phosphoinositide 3-kinase)/Akt pathway, particularly by its major activators insulin and IGF-1 (insulin-like growth factor-1), is a powerful integrator of physiological responses rudimentary to successful aging.
-
Diabetic encephalopathy is now accepted as an important complication of diabetes.
-
Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are devastating neurodegenerative disorders with clinical, genetic, and neuropathological overlap.
-
Glial proliferation and activation are associated with disease progression in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar dementia.
-
Amyloid precursor protein (APP) proteolysis is required for production of amyloid-β (Aβ) peptides that comprise β-amyloid plaques in brains of Alzheimer's disease (AD) patients.
-
γ-Secretase is an intramembrane aspartyl protease that cleaves the amyloid precursor protein to produce neurotoxic β-amyloid peptides (i.e. Aβ42) that have been implicated in the pathogenesis of Alzheimer disease.
-
59/100
Expansion of a GGGGCC hexanucleotide repeat upstream of the C9orf72 coding region is the most common cause of familial frontotemporal lobar degeneration and amyotrophic lateral sclerosis (FTLD/ALS), but the pathomechanisms involved are unknown.
-
Soluble oligomers of the amyloid-β (Aβ) peptide cause neurotoxicity, synaptic dysfunction, and memory impairments that underlie Alzheimer disease (AD).
-
Transactivating response region DNA binding protein (TDP-43) is the major protein component of ubiquitinated inclusions found in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) with ubiquitinated inclusions.
-
40/100
The RCAN1 gene encodes three different protein isoforms: RCAN1-4, RCAN1-1L, and RCAN1-1S. RCAN1-1L is the RCAN1 isoform predominantly expressed in human brains.
-
A hallmark of Alzheimer disease (AD) is the accumulation of the amyloid-β (Aβ) peptide in the brain.
-
Alzheimer's disease (AD) is the most common cause of dementia worldwide.
From across this tag
9 of the 1,159 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.
- Hippocampal T cell infiltration promotes neuroinflammation and cognitive decline in a mouse model of tauopathy
- Intranasal oxytocin for apathy in people with frontotemporal dementia (FOXY): a multicentre, randomised, double-blind, placebo-controlled, adaptive, crossover, phase 2a/2b superiority trial
- TGF-β Pathway–Based Polygenic Risk Score Modifies the Association between Red Meat Intake and Colorectal Cancer Risk: Application of a Novel Pathway-Based PRS Method
- Perineuronal net digestion with chondroitinase restores memory in mice with tau pathology
- Loss of C9ORF72 impairs autophagy and synergizes with polyQ Ataxin-2 to induce motor neuron dysfunction and cell death
- Functional and dynamic polymerization of the ALS-linked protein TDP-43 antagonizes its pathologic aggregation
- Identifying natural inhibitors against FUS protein in dementia through machine learning, molecular docking, and dynamics simulation
- TDP-43 and FUS RNA-binding proteins bind distinct sets of cytoplasmic messenger RNAs and differently regulate their post-transcriptional fate in motoneuron-like cells
- Galectin-3, a rising star in modulating microglia activation under conditions of neurodegeneration