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.
-
Sixteen patients with progressive language disorder have been studied longitudinally.
Why it matters
This study of 16 patients describes progressive language disorder due to lobar atrophy, with autopsy findings showing no senile plaques or neurofibrillary tangles. The authors argue this condition is part of a spectrum of non-Alzheimer lobar atrophy, so it does not concern treating or preventing Alzheimer's disease.
-
Hallmarks of central nervous system (CNS) disease in AIDS patients are headaches, fever, subtle cognitive changes, abnormal reflexes, and ataxia.
Why it matters
This review describes nervous system disease in AIDS, including dementia, inflammation and microglial nodules. It concerns HIV-associated disease, not Alzheimer's disease, and reports no treatment or cure.
-
Localization of beta-2 integrins in normal and Alzheimer disease temporal cortex was studied immunohistochemically.
Why it matters
Microglia, the brain's resident immune cells, were found to carry immune-cell surface markers (CD11a, CD11b, CD11c, CD18, leukocyte common antigen and Fc gamma RI) even in normal temporal cortex, and these markers stained more intensely on reactive microglia in Alzheimer's tissue. HLA-DR, seen "on only a few microglia in control tissue", was "intensely expressed on large numbers of reactive microglia in Alzheimer tissue." This is a tissue-staining study that shows an association, not a cause, and it reports no treatment, cure or prevention result.
-
The plasma distribution of gallium (as an analogue of aluminium) was investigated in patients with Alzheimer disease, Down syndrome, or stroke dementia, in subjects on haemodialysis for chronic renal failure, and in healthy controls.
Why it matters
Plasma gallium-transferrin binding was significantly lower in people with Alzheimer's disease and Down syndrome than in controls, which the authors suggest could allow more unbound aluminium to enter the brain. This is an observational blood study and does not test whether reducing aluminium affects the disease.
-
We retrospectively analyzed the charts of 58 long-term survivors of small-cell lung cancer (SCLC) (greater than 2 years) for neurological complications and their impact on the well-being of these patients.
Why it matters
This retrospective study of 58 long-term small-cell lung cancer survivors found that prophylactic cranial irradiation reduced CNS metastasis but that in only two patients did it appear responsible for progressive dementia. It concerns cancer treatment complications, not the treatment, cure, or prevention of Alzheimer's disease.
-
The gene encoding the beta-amyloid precursor protein has been assigned to human chromosome 21, as has a gene responsible for at least some cases of familial Alzheimer disease.
Why it matters
This mapping study located the beta-amyloid precursor protein gene on chromosome 21 near the region that causes Down syndrome when trisomic. It is basic genetics and provides no treatment, cure or prevention for Alzheimer's disease.
-
Combined neuropathological and neurochemical assessment of the nucleus of Meynert in senile dementia of Alzheimer type (SDAT) have demonstrated that the cholinergic biochemical activity, choline acetyltransferase, is more extensively reduced in the nucleus (over 90%) than the loss of putative cholinergic perikarya (35%).
Why it matters
In brain tissue from people with senile dementia of Alzheimer type, cholinergic biochemical activity was reduced more than the loss of cholinergic cells, suggesting degeneration of cholinergic axons to the cortex. This is a descriptive pathology study and reports no treatment, cure or prevention.
-
Down syndrome (trisomy 21) is the most common genetic cause of intellectual disability.
-
Across both regions, no evidence of reduced total neuronal density was observed, but a modest reduction in parvalbumin interneurons was observed in the cingulate gyrus, and there were only modest reductions in some synaptic markers in DLB.
Why it matters
This study found no evidence of reduced total neuronal density and only modest reductions in some synaptic markers in dementia with Lewy bodies, and Lewy body burden was not associated with any synaptic marker abundance or neuronal density. The authors conclude that the link between α-synuclein proteinopathy and disease requires further investigation, and no treatment, cure or prevention is reported.
-
43/100
α -Syn positivity was detected in 9% of CU individuals, a lower rate than in clinically impaired participants with AD (16%) and LBD diagnoses (81%).
Why it matters
Among cognitively unimpaired individuals, 9% had α-synuclein positivity, and these people were older, had lower synaptic integrity, and performed worse on executive function and working memory tests. The authors say further work is needed to understand the timeline of changes and heterogeneity in progression.
-
Tauopathies, such as Alzheimer's disease and frontotemporal dementia, are common neurodegenerative diseases characterized by misfolding, hyperphosphorylation, and aggregation of tau.
Why it matters
Human induced pluripotent stem cell-derived neurons engineered to express adult 4R tau isoforms developed seeding-competent, hyperphosphorylated tau in tangle-like structures without added tau pathology. The model can be used to test chemical disease modulators and evaluate human tau PET tracers, but it is a cell model, not a treatment or cure.
-
Vascular cognitive impairment and dementia (VCID) is increasingly recognized as one of the leading causes of cognitive decline in aging populations.
Why it matters
This review discusses how oxidized LDL may contribute to blood vessel damage, inflammation and cognitive decline in vascular cognitive impairment and dementia. It outlines mechanisms rather than testing a treatment.
-
43/100
Here, we show that cofilin is hyper-phosphorylated in human ALS and disease models compared to controls.
Why it matters
This study found that cofilin is hyper-phosphorylated in human ALS and disease models, disrupting actin dynamics and triggering TDP-43 pathology. Treatment with the S3A peptide prevented features of TDP-43 pathology and apoptosis in neuronal cells, but this is early-stage and not yet tested in patients.
-
43/100
This method differentiated eight tauopathies, including Alzheimer's disease, Pick disease, progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), argyrophilic grain disease (AGD), frontotemporal dementia with parkinsonism associated with chromosome 17 with N279K mutation (FTDP-17 N279K), and globular glial tauopathies types II and III.
Why it matters
A salt-modulated, heparin-free RT-QuIC method distinguished eight tauopathies, including Alzheimer's disease, based on strain-specific aggregation kinetics and structure. This is a laboratory diagnostic tool, not a treatment, cure or prevention.
-
Late-onset Alzheimer disease (LOAD), the most common form of dementia among older adults, is a neurodegenerative disease characterized by brain amyloid-β (Aβ) plaque deposition and neurofibrillary tangles.
Why it matters
This study characterized T-cell receptor sequence diversity and HLA alleles from peripheral tissue DNA of 72 Midwestern Amish participants in longitudinal aging studies, based on evidence implicating the adaptive immune system in late-onset Alzheimer's disease. It is an early immune-focused investigation and does not establish a treatment, cure, or prevention.
-
hexanucleotide repeat expansions (HRE) and WMH in bvFTD patients. bvFTD and svPPA are associated with elevated WMH burden independent of CVRF.
Why it matters
People with behavioral variant frontotemporal dementia and semantic variant primary progressive aphasia had more white matter hyperintensities than expected, even without cardiovascular risk factors. This was a small, single-center, retrospective study, so it does not provide a treatment or prevention approach.
-
Alzheimer's disease (AD) represents the most common cause of dementia and urgently requires sensitive biomarkers and effective therapies.
Why it matters
Microglia-derived extracellular vesicles from the cerebrospinal fluid of Alzheimer's patients carried microRNAs that activated the RNA sensor TLR8 and triggered inflammatory responses from microglia in laboratory experiments. This is early cellular research and does not show that targeting these vesicles would treat or prevent Alzheimer's disease.
-
Each 1-SD increase in eGDR was significantly associated with a reduction in WMH volume (β = -0.057; 95% CI: -0.062 to -0.051; p 0.05).
Why it matters
In this large prospective cohort, each 1-SD increase in estimated glucose disposal rate was associated with a reduction in white matter hyperintensity volume. Lower eGDR was linked to greater WMH burden, suggesting it may help predict this burden, but the study does not test whether improving eGDR prevents dementia.
-
We identified 51 transcriptome-wide significant (edgeR q < 0.05) DEGs, compared to controls, and 26 transcriptome-wide significant DEGs, compared to PD, in PDD plasma SEV.
Why it matters
This study identified RNA biomarkers in plasma small extracellular vesicles that could distinguish Parkinson's disease dementia from Parkinson's disease with at least 80% sensitivity and specificity. The authors note that future research on the identified pathways may help find new therapeutic targets, but no treatment is tested here.
-
Overall PiB-PET uptake increased during the first two years (before ARIA-E) and decreased during the last two years (including ARIA-E episodes) (0.03±0.05 vs. -0.04±0.04 SUVR/year, p-value=0.01, Figure 2).
Why it matters
In one DIAN-TU-001 participant treated with gantenerumab, PiB-PET uptake decreased during the years including ARIA-E episodes, and the ARIA-E region showed lower amyloid area fraction at autopsy. These are preliminary single-case imaging-neuropathology findings about ARIA-E and local amyloid removal, not evidence of a cure or prevention.
-
PSMD was more strongly associated with age in DS (rho=0.56; p <0.001) than in HC (rho=0.38, p <0.001; Figure 1A), with regression lines starting to diverge at age 42.
Why it matters
This cross-sectional study found that a diffusion imaging marker of white matter damage increased along the Alzheimer's continuum in people with Down syndrome and changed about 10-15 years before symptoms. It suggests the marker may help detect early white matter changes, but it does not test any treatment, cure or prevention.
-
Among 1,307 individuals, 36.9% were non-White and 49.7% were women.
Why it matters
In a brain bank of 1,307 individuals, hippocampal sclerosis was strongly associated with TDP-43 pathology, but its positive predictive value for TDP-43 pathology was only 48.8%, rising to 59.4% among cognitively impaired individuals, and vascular pathology also played a significant role. The authors conclude this limits its predictive value for LATE-NC and call for further research, so it does not provide a treatment, cure or prevention.
-
Down syndrome (DS) stands out as the most prevalent genetic contributor to intellectual disability, marked by the presence of an extra copy of chromosome 21 (HSA21).
Why it matters
Protein analysis of post-mortem frontal cortex found distinct proteome signatures in Down syndrome before and after Alzheimer's pathology, affecting pathways related to energy processes, synaptic transmission and stress response. The authors say these data support a genotype effect that promotes Alzheimer's-related protein changes, but this is tissue analysis and no treatment is tested.
-
M1 specifically enhanced uptake of Aβ fibrils through reduction of intracellular cAMP levels, without affecting monomeric or oligomeric Aβ internalization.
Why it matters
This study found that selective agonism of GPR34 with M1 enhanced microglial uptake of Aβ fibrils in vitro and increased microglial Aβ uptake in vivo in a way that required functional TREM2 signaling, while GPR34 expression was reduced in microglia from Alzheimer's patients and declined with age. The authors identify GPR34 as a promising therapeutic target, but this is preclinical work and no treatment has been tested in patients.
-
The concomitant depletion of dopaminergic and serotonergic inputs within the hippocampus of C57BL/6N mice provokes a pronounced activation of microglia via the NLRP3-inflammasome pathway, accompanied by increased IL-1β expression.
Why it matters
In mice, damage to midbrain dopamine and serotonin inputs triggered microglial activation and worsened amyloid and tau pathology, while L-DOPA or fluoxetine reduced astrocyte reactivity and tau hyperphosphorylation. These findings are from animal experiments and suggest a possible link to faster dementia progression in people with midbrain deficits, but they do not show a treatment for patients.
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.
- G-quadruplex-binding small molecules ameliorate C9orf72 FTD/ALS pathology in vitro and in vivo
- Plasma neurofilament light chain in relation to 10-year change in cognition and neuroimaging markers: a population-based study
- Crucial role of microglia-mediated myelin sheath damage in vascular dementia: Antecedents and consequences
- Genetic etiology of Parkinson disease associated with mutations in the SNCA, PARK2, PINK1, PARK7, and LRRK2 genes: a mutation update
- Plasma Biomarkers and Disease Prognosis in Mild Cognitive Impairment with Lewy Bodies
- Inhibition of tau aggregation in a novel Caenorhabditis elegans model of tauopathy mitigates proteotoxicity
- Redox proteomic analysis of carbonylated brain proteins in mild cognitive impairment and early Alzheimer's disease
- Human Interleukin-34 facilitates microglia-like cell differentiation and persistent HIV-1 infection in humanized mice
- Mitochondrial ATP-synthase in the entorhinal cortex is a target of oxidative stress at stages I/II of Alzheimer's disease pathology
- Modelling synaptic dysfunction in childhood dementia using human iPSC-derived cortical networks