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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The antigenic profile of neurofibrillary tangles (NFT) in Alzheimer's disease (AD), senile dementia of Alzheimer type (SDAT), progressive supranuclear palsy (PSP) and in non-demented aged humans was investigated by light and electron microscopic immunocytochemistry using antisera and monoclonal antibodies to tubulin, microtubule-associated proteins (MAP1, MAP2 and tau), neurofilament proteins and determinants unique to Alzheimer paired helical filaments (PHF).
Why it matters
This laboratory study found that phosphorylated tau is a major component of neurofibrillary tangles in both Alzheimer's disease and progressive supranuclear palsy, though at least one tangle feature differs between them. It is basic brain tissue research and does not provide a treatment, cure, or prevention.
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The Mediterranean diet, rich in plant-based foods, olive oil, and fish, has been consistently associated with slower cognitive decline and reduced risk of neurodegeneration in observational studies and some clinical trials.
Why it matters
This review reports that the Mediterranean diet has been consistently associated with slower cognitive decline and reduced neurodegeneration risk in observational studies and some clinical trials. More trials and improved multi-omics systems are needed before these findings can be applied in clinical practice.
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Inter-organelle contact sites are key hubs for organelle bidirectional crosstalk.
Why it matters
This study identified that reactive oxygen species promote TDP-43 localization to RNA granules via oxidation at specific cysteine sites, and that this dynamic crosstalk has consequences for ALS and FTD. These findings are from super-resolution live microscopy and describe a mechanism, not a treatment.
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Alzheimer's disease (AD) affects over 55 million people worldwide and lacks effective disease-modifying therapies targeting neuroinflammation.
Why it matters
This is a computational analysis of existing human brain data that identifies SYK kinase as a possible drug target and lists candidate inhibitors, so it does not test any treatment in patients. No clinical benefit, cure or prevention is shown.
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41/100
TDP-43 and FUS are RNA-binding proteins involved in the regulation of diverse RNA-processing events and have been strongly implicated in neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).
Why it matters
This laboratory study shows that TDP-43 and FUS contribute to transcription termination through the R1810me2s-SMN pathway, and that disruption of their recruitment leads to defective RNA polymerase II termination, R-loop accumulation and DNA damage. It establishes a mechanistic link between these proteins and transcription termination but does not test any treatment, cure or prevention.
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Obesity and its associated metabolic disturbances increase the risk of cognitive decline, dementia, and anxiety-related disorders.
Why it matters
In rats fed a high-fat high-sucrose diet, chronic caffeine reduced memory and cognitive deficits and anxiety, linked to changes in hippocampal signaling and reduced neuroinflammation. This is animal research, so it does not show that caffeine prevents cognitive decline or dementia in people.
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Hippocampal pan-histone H3 crotonylation (H3Kcr) and H3K18cr were significantly upregulated in both 5xFAD and Aβ42-injected mice compared to controls.
Why it matters
In mice and cells, elevated microglial H3K18cr promoted STAT1 expression and neuroinflammation, and fludarabine suppressed STAT1 and reduced pro-inflammatory cytokines. This is early animal and cell research, so it does not show a treatment or prevention for Alzheimer's disease in humans.
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Control and LOAD hiPSCs exhibited comparable efficiency in forming brain capillary endothelial-like cells (BCECs).
Why it matters
In cells grown from people with late-onset Alzheimer's disease, the blood-brain barrier showed subtle changes in barrier-related genes and reduced transport of amyloid beta, though barrier tightness itself was not significantly different. This is a laboratory model that may be useful for future studies aiming to correct these changes, not a treatment.
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Alzheimer disease (AD) is a major health issue of global concern whereby there are minimal treatment options.
Why it matters
This review proposes that the dietary carotenoid lutein could act as a 'molecular sponge' neutralizing toxic aldehydes such as 4-HNE and acrolein that injure neurons. This is a hypothesis about a possible mechanism, not evidence that lutein treats, cures, or prevents Alzheimer's disease.
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Frontotemporal dementia (FTD) is a group of early onset and progressive disorders, characterized by degeneration in the frontal and temporal lobes, and subsequent deterioration in cognition, personality, social behavior, and language, with aggregates of the RNA-binding protein TDP-43 being present in ~45% of the cases.
Why it matters
In a TDP-43 overexpressing mouse model of frontotemporal dementia, this study found alterations in the small intestinal endocannabinoidome, oxylipins and, preliminarily, the gut microbiome compared with wildtype mice. These are animal findings about intestinal signaling and no treatment, cure or prevention for Alzheimer's disease is tested.
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Aggregation of the microtubule-binding protein tau is the histopathological hallmark of Alzheimer's disease (AD) and other neurodegenerative diseases, which are collectively known as tauopathies.
Why it matters
Two chemical analogs of CNS-11 disaggregated tau fibrils from Alzheimer's patient brains in the laboratory and reduced insoluble tau in a mouse model of tauopathy after 8 weeks of treatment. This is early laboratory and animal research, so it is not yet known whether these molecules would be safe or effective in people.
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Plasma Aβ levels and regional WMH burden are associated with glymphatic dysfunction as indicated by reduced ALPS.
Why it matters
Across the Alzheimer's continuum, a lower glymphatic function index was found in Alzheimer's patients and correlated with regional white matter hyperintensity volumes and plasma amyloid-β42/40 ratios. This links glymphatic dysfunction to small vessel disease and amyloid markers, but it is an observational study and does not test treatment or prevention.
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= 0.14. The effect of ADI score was also significant, β = -0.36, t = -2.30, p < .05; while the effect of RUCC, β = 0.06, t = 0.34, p = .73, and the interaction between ADI and RUCC, β = -0.001, t = 0.27, p = .99, were nonsignificant.
Why it matters
In people with schizophrenia, living in a more environmentally deprived neighborhood predicted worse cognitive impairment. The authors suggest this means environment-focused approaches should be considered when treating cognitive impairment in schizophrenia, though the study was cross-sectional and cannot show cause and effect.
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Alzheimer's disease (AD) and dementia with Lewy bodies (DLB) are the two most common forms of dementia due to neurodegeneration.
Why it matters
This review compares the molecular and pathological features of Alzheimer's disease and dementia with Lewy bodies and discusses emerging biomarkers. It is a discussion of shared and distinct biology, not a treatment or cure.
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The first SVD component accounted for 21.56%, 12.93%, 11.91% of the total co-variability between the pairs (cortical thickness, tau), (relative GM density, tau) and (absolute GM density, tau), respectively.
Why it matters
In this cross-sectional imaging study of people with mild cognitive impairment, tau was associated with atrophy patterns across different imaging biomarkers independently of beta-amyloid burden and APOE ε4 genotype. The findings suggest tau plays a significant role in neurodegeneration in MCI.
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Average age of participants was 66 (21-88) years. 25 were biologically female and 15 were amyloid positive.
Why it matters
This study found that off-target signal outside the brain was more pronounced and widespread with the tau PET tracer 18F-MK-6240 than with 18F-AV-1451. This signal could affect tau PET quantification that uses a cerebellar reference region, and more work is needed to understand what contributes to it.
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In both cohorts there were significant associations between CSF MTBR-tau243 and the temporal meta-ROI (BioFINDER-2: t = 17.1, p < 0.001, Knight-ADRC: t=11.0, p <0.001).
Why it matters
This study found that the relationship between tau PET and a spinal fluid marker of tau did not differ by sex across two cohorts. It is an observational biomarker study and does not test any treatment, cure, or prevention.
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Vascular dementia is the second most common form of dementia.
Why it matters
This is a computer-based (in silico) study that screened small molecules for inhibiting HDAC3 as a possible approach to vascular dementia, selecting two top compounds based on docking and simulation. It is early computational work and no compound has been tested in patients, so it does not yet show any treatment, cure or prevention.
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Our multi-omics study revealed distinct gut microbiota and metabolite alterations in PD patients with cognitive impairment, highlighting gut-brain axis dysfunction.
Why it matters
This multi-omics study found that Parkinson's disease patients with mild cognitive impairment had distinct gut microbial and metabolic profiles compared with those with normal cognition. It identifies phenylacetylglutamine as a promising biomarker for Parkinson's disease mild cognitive impairment, which is about diagnosis rather than treating or preventing Alzheimer's.
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We estimated the overall concentration (mean standardized values) and principal components (PCs) of the proteomics and lipidomics data independently.
Why it matters
This multi-omics study found that overall cerebrospinal fluid protein and lipid concentrations were strongly associated with CSF p-tau181 and Aβ42 levels, and that a genetic variant in GMNC was linked to these metrics. The authors suggest CSF production and clearance rates may contribute to biomarker variability, which has implications for how neurodegeneration studies are interpreted, but no treatment, prevention or cure is reported.
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TDP-43 seeding activity was detected in 67% of TDP-43-linked symptomatic patients, with a specificity of 93%.
Why it matters
A seed amplification assay detected misfolded TDP-43 in the cerebrospinal fluid of 67% of symptomatic patients with genetic FTD/ALS and in almost half of presymptomatic carriers, mostly with GRN mutations. Two presymptomatic GRN carriers who tested positive later developed symptoms, suggesting a possible link between a positive test and conversion to the symptomatic phase.
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Our results suggest that microglial activation is a major phenomenon linking Aβ and astrocyte reactivity in the living AD brain.
Why it matters
In people across the aging and Alzheimer's clinical spectrum, amyloid pathology was associated with astrocyte reactivity only when microglial activation was also elevated. This supports microglia as a factor in how amyloid affects astrocytes, but it does not test or establish any treatment.
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41/100
Higher education was associated with lower vascular risk (p < 0.001) and WMH burden (p = 0.004).
Why it matters
Higher education was linked to lower vascular risk and less white matter hyperintensity burden, with vascular risk factors explaining part of this relationship. The authors suggest addressing vascular health may reduce white matter hyperintensities, but this is an observational finding and not a tested intervention.
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Alzheimer’s disease (AD) is the leading cause of dementia in elderly individuals worldwide; however, all mechanisms leading to disease onset and progression are not well understood.
Why it matters
In a transgenic rat model of human-like tauopathy, single-cell and spatial transcriptomics revealed changes in cell communication involving glutamatergic transmission and Netrin signaling. The study reinforces that synaptic dysfunction is an early event and highlights potential targets, but it is animal model work.
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41/100
Synaptic loss is strongly associated with cognitive decline in Alzheimer's disease (AD).
Why it matters
In two Alzheimer's-like mouse models, inhibiting LMTK1 restored neurite growth, synaptic density, long-term potentiation and cognitive function, and human genomic data supported LMTK1's involvement in cognition. This is animal and database research, so it is not yet known whether inhibiting LMTK1 would help people with Alzheimer's disease.
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.
- Microglia: biology and pathology
- Nonapoptotic neurodegeneration in a transgenic mouse model of Huntington's disease
- Apolipoprotein E epsilon 4 allele and hippocampal volume in twins with normal cognition
- Dietary docosahexaenoic acid and docosapentaenoic acid ameliorate amyloid-beta and tau pathology via a mechanism involving presenilin 1 levels
- Systematic analysis of cellular cross-talk reveals a role for SEMA6D-TREM2 regulating microglial function in Alzheimer’s disease
- pH-dependent binding of synthetic beta-amyloid peptides to glycosaminoglycans
- Amyotrophic lateral sclerosis
- Cofilin hyperphosphorylation triggers TDP-43 pathology in sporadic amyotrophic lateral sclerosis
- Neuroprotective epi-drugs quench the inflammatory response and microglial/macrophage activation in a mouse model of permanent brain ischemia
- A Comprehensive Profile of ChIP-Seq-Based PU.1/Spi1 Target Genes in Microglia