Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Highest usefulness score first. Studies without a score come last.
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NAD(P)H quinone oxidoreductase 1 (NQO1) is a multi-functional protein that catalyses the reduction of quinones (and other molecules), thus playing roles in xenobiotic detoxification and redox balance, and also has roles in stabilising apoptosis regulators such as p53.
Why it matters
This review describes a common form of the NQO1 protein that is associated with increased cancer risk and certain neurological disorders including Alzheimer's disease, possibly through its role in antioxidant defence. It suggests that correcting NQO1 misfolding with pharmacological chaperones is a possible strategy, but this has not been tested as an Alzheimer's treatment.
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Cerebral amyloid angiopathy (CAA) results from amyloid-β deposition in the cerebrovasculature.
Why it matters
In a mouse model of cerebral amyloid angiopathy, oral taxifolin improved cerebral blood flow, promoted amyloid-β removal, and prevented cognitive dysfunction. This is an early animal study and does not yet show a treatment, cure, or prevention for Alzheimer's disease in people.
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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).
Why it matters
This study used humanized mice to show that Interleukin-34 supports microglia-like cell differentiation and persistent HIV-1 infection in the brain. It does not test any treatment, cure, or prevention for 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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Cerebrovascular pathology is a significant mediator in Alzheimer's disease (AD) in the general population.
Why it matters
In autopsy brain tissue, small bleeds and cerebral amyloid angiopathy were more common in Down syndrome and appeared to contribute to dementia. The authors say these are targets for future clinical trials, so no treatment is established yet.
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These findings provide compelling evidence that misfolded or pathological conformers of tau undergo cell-to-cell spread in a tauopathy strain-specific manner.
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These results are especially relevant when compared to previous SSD studies showing effects in behavior only after a demanding cognitive training.
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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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N -acetylcysteine (NAC), which is an acetylated cysteine compound, has aroused scientific interest for decades due to its important medical applications.
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Alzheimer disease (AD) is a complex pathology related to multiple causes including oxidative stress.
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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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The progression of tau pathology in Alzheimer's disease follows a stereotyped pattern, and recent evidence suggests a role of synaptic connections in this process.
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This study proposes TLR2 immunotherapy as a novel therapeutic strategy for synucleinopathies of the aging population.
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41/100
Frontotemporal dementia and amyotrophic lateral sclerosis patients with C9orf72 mutation show cytoplasmic poly-GR and poly-PR aggregates.
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Diffusion-tensor imaging (DTI) is a noninvasive medical imaging tool used to investigate the structure of white matter.
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In vivo 11 C-PBB3 binding to the rTg4510 neocortex/hippocampus was increased relative to controls and correlated with local atrophy.
Why it matters
This study in tauopathy mouse models compared in-vitro and in-vivo measures of tau deposits and their link to brain atrophy. It is animal research into how tau relates to nerve cell loss and does not test a treatment, cure or prevention for Alzheimer's disease in people.
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Accumulating evidence suggests that brain-derived neurotrophic factor (BDNF) is associated with the pathophysiology of major depressive disorder (MDD).
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Alzheimer's disease (AD) is the most common cause of dementia in the elderly.
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Aging is a major driving force underlying dementia, such as that caused by Alzheimer's disease (AD).
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Synucleinopathies, such as Parkinson's disease and dementia with Lewy bodies, are neurodegenerative disorders that are characterized by the accumulation of α-synuclein (aSyn) in intracellular inclusions known as Lewy bodies.
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Clearance of amyloid-beta (Aβ) from the brain is an important therapeutic strategy for Alzheimer's disease (AD).
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In vivo exploration of activated microglia in neurodegenerative diseases is achievable by Positron Emission Tomography (PET) imaging, using dedicated radiopharmaceuticals targeting the translocator protein-18 kDa (TSPO).
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Apolipoprotein E4 (E4) and type 2 diabetes are major risk factors for cognitive decline and late onset Alzheimer's disease (AD).
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It is well-established that inflammation plays an important role in Alzheimer's disease (AD) and frontotemporal lobar dementia (FTLD).
From across this topic
10 of the 4,748 studies in this topic, 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.
- Transcriptome and metabolome analysis of crGART, a novel cell model of de novo purine synthesis deficiency: Alterations in CD36 expression and activity
- Soluble oligomers of amyloid-β peptide disrupt membrane trafficking of α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor contributing to early synapse dysfunction
- Glucose regulation, cognition, and brain MRI in type 2 diabetes: a systematic review
- TDP-43 is intrinsically aggregation-prone, and amyotrophic lateral sclerosis-linked mutations accelerate aggregation and increase toxicity
- Small molecule JRMS modulating importin-β1 chaperone activity as a therapeutic strategy reducing TDP-43 pathology
- Cognitively normal APOE ε4 carriers have specific elevation of CSF SNAP-25
- Elucidating the Role of Cerebellar Synaptic Dysfunction in C9orf72-ALS/FTD - a Systematic Review and Meta-Analysis
- Mechanism of STMN2 cryptic splice-polyadenylation and its correction for TDP-43 proteinopathies
- The role of exercise-induced myokines in muscle homeostasis and the defense against chronic diseases
- 24(S)-hydroxycholesterol participates in a liver X receptor-controlled pathway in astrocytes that regulates apolipoprotein E-mediated cholesterol efflux