Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Download bibliography of all 4,766 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
-
Stroke and dementia are leading causes of death and disability worldwide, requiring enhanced preventive strategies.
Why it matters
This study used genetic methods to look at whether GLP-1 receptor agonists might affect stroke and Alzheimer's disease across different ancestries. The text provided does not report any results, so no conclusion about treating or preventing Alzheimer's disease can be drawn from it.
-
Hierarchical linear regression was used to assess an incremental contribution of the set of inflammatory markers’ PRS to explaining VF variance compared to the null model.
Why it matters
In people with recent-onset or chronic schizophrenia, genetic scores for inflammatory markers did not significantly improve prediction of verbal fluency. An Alzheimer polygenic risk score was a significant predictor of verbal fluency only in the chronic schizophrenia group, but this finding is about schizophrenia, not Alzheimer disease treatment or prevention.
-
Tauopathies are neurodegenerative diseases characterized by the accumulation of misfolded tau protein and include Alzheimer's disease (AD) and related dementia disorders.
Why it matters
In worm and cell models, loss of the gene smrd-1/SMARCAD1 reduced tau levels and rescued tau-related neuronal dysfunction and neurodegeneration by lowering tau mRNA. This is laboratory work, and human brain tissue showed SMARCAD1 depletion in only a subset of cases, so it is not yet a treatment for people.
-
The NfL assay met analytical criteria, with precision demonstrating coefficients of variation <3% across runs, a lower limit of quantification of 3.10 pg/mL, linearity with <12% deviation, and <10% interference.
Why it matters
A fully automated plasma neurofilament light chain assay met analytical criteria and showed elevated NfL in Alzheimer's disease and multiple sclerosis patients compared with controls. This supports use of the assay in research and clinical laboratories, but NfL is not specific to Alzheimer's disease.
-
Dietary supplement silver nanoparticles have recently drawn attention following reports of hazards associated with long-term use.
Why it matters
In mice, long-term dietary silver nanoparticles caused Alzheimer-like brain changes by depleting gut bacteria, and supplementing with Bifidobacterium breve reduced these changes. This is animal research only, so it does not show that silver nanoparticles cause Alzheimer's in people or that probiotics prevent it.
-
Vascular dementia is a common cognitive disorder that is often triggered by neuroinflammatory responses caused by cerebrovascular injury, which further exacerbates the progression of the disease.
Why it matters
In a rat model of vascular dementia, microglial SHP2 appeared to inhibit disease progression by suppressing a neuroinflammatory signaling pathway. These are animal findings, so it is not known whether targeting SHP2 would help people with vascular dementia.
-
We identified four SNPs (rs335929, rs335930, rs335931 and rs455671) were significantly associated with CSVD presence.
Why it matters
In clinical and mouse work, reduced AQP4 expression was associated with cerebral small vessel disease, and Aqp4-deficient mice showed worse white matter injury that appeared mediated by upregulation of complement component 3. Targeting C3 activation is suggested as a possible strategy, but this is early experimental research and not an established treatment.
-
Intramembrane proteolysis by γ-secretase is critically implicated in Alzheimer disease pathogenesis by processing of its amyloid precursor protein substrate C99 into harmful amyloid-β peptide (Aβ) species.
Why it matters
This laboratory study shows that interactions between the C99 N-terminal region and gamma-secretase exosites affect substrate cleavage, and that interfering with these interactions can modulate amyloidogenic processing. It suggests a possible approach for lowering amyloid-beta generation, but no treatment in humans is tested.
-
35/100
Lipoprotein(a) [Lp(a)] is a genetically determined lipoprotein particle composed of apolipoprotein B-100 covalently linked to apolipoprotein(a) [apo(a)] via a disulfide bond.
Why it matters
This review is about lipoprotein(a) and cardiovascular risk, not Alzheimer's disease, so it provides no information on Alzheimer's treatment, cure or prevention. It describes experimental therapies that lower lipoprotein(a) and notes that large outcome trials are still underway.
-
We observed higher within‐ and between‐DMN FC in the CS‐OSA compared to the CI‐OSA group; however, this difference was not observed between the CS‐nonOSA and CI‐nonOSA groups.
Why it matters
Brain scans of seventy-five older adults with Down syndrome from the ABC-DS study showed that sleep apnea interacted with cognitive status in shaping how strongly key brain networks communicate. Among people with sleep apnea, those who were still cognitively stable had higher connectivity in the default mode network than those with cognitive impairment, a gap not seen in people without sleep apnea. The authors suggest connectivity may first rise and then fall as Alzheimer's symptoms begin in people with Down syndrome and sleep apnea.
-
We have shown that B6 and WSB genetic backgrounds are less susceptible to CAA compared to BXW, which develops robust CAA.
Why it matters
In different mouse strains, this study found that genetic background affects susceptibility to cerebral amyloid angiopathy, with BXW mice developing robust CAA and showing more IBA+ area per plaque, while WSB mice had fewer but larger plaques and less GFAP+ area per plaque. These are preliminary animal findings about microglia and astrocytes, and no treatment, cure or prevention for Alzheimer's disease is tested.
-
The different Alzheimer and Pick tau folds establish the existence of molecular conformers of assembled tau.
Why it matters
This work describes distinct molecular folds of assembled tau in different tauopathies, including Alzheimer's disease, Pick's disease and chronic traumatic encephalopathy. The authors report forming the Alzheimer fold in the test tube from truncated or modified human tau, which is laboratory structural work with no treatment or prevention tested.
-
Perturbations in the metabolism of microtubule‐associated protein tau (tau) underlie the pathology of a broad array of dementias, including chronic traumatic encephalopathy, amyotrophic lateral sclerosis (ALS) with cognitive impairment (ALSci) and approximately half of the dementias associated with frontotemporal lobar degeneration.
Why it matters
This cell-based study showed that extracellular vesicles can transfer tau and TDP-43 proteins to recipient cells, where they co-localize. These findings further understanding of how tau and TDP-43 may interact and co-aggregate, but they are preliminary and not yet applicable to treatment.
-
Chronic cerebral hypoperfusion (CCH) profoundly affects patient well-being and has been proposed as a risk factor for cognitive impairment and dementia.
Why it matters
In a rat model of chronic cerebral hypoperfusion, the drug clemastine prevented myelin loss, synaptic loss and cognitive deficits. These are animal results only, and the authors describe clemastine as a promising option that still needs testing in humans.
-
Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are progressive neurodegenerative diseases characterised by nuclear TDP-43 loss.
Why it matters
This study developed an ultrasensitive RT-qPCR assay targeting STMN2 cryptic exon that detected a 42-fold increase in ALS motor cortex previously missed by conventional primers, with detection set at 0.16% deficient cells. It is a measurement tool for research and drug studies and does not itself test any treatment, cure or prevention.
-
Previous observational studies demonstrated that lung cancer and both Alzheimer disease (AD) and Parkinson disease (PD) may be related.
Why it matters
This genetic analysis found that lung squamous cell carcinoma was negatively related to Alzheimer's disease, meaning it was associated with lower risk. The findings come from statistical genetic methods and do not show that having or treating lung cancer would prevent or cure Alzheimer's disease.
-
DNA methylation, mRNA and protein levels, and cognitive performance using the Mini-Mental State Examination (MMSE) and Clock Drawing Test (CDT).
Why it matters
This study examined BDNF methylation, mRNA and protein levels in blood and found some links to dementia severity and cognitive test scores. The authors say further studies are needed to evaluate whether these blood markers have practical use, and no treatment was tested.
-
Bridging Integrator 1 (BIN1) is a genetic risk factor for late-onset Alzheimer disease.
Why it matters
This biophysical study identified the neuronal scaffold protein p140Cap as a BIN1 SH3 domain-interacting protein and found that a rare BIN1 coding variant significantly reduces p140Cap and tau binding. The work characterizes a molecular interaction related to a late-onset Alzheimer's risk gene, but it does not test any treatment, cure or prevention.
-
Cerebral small vessel disease (cSVD) is a major cause of vascular dementia and stroke.
Why it matters
This zebrafish study found that loss of col4a1 reproduced features of cerebral small vessel disease, including spontaneous brain hemorrhage and cerebrovascular abnormalities, and that blocking mmp9 reduced some of these effects. Because this is an animal model, the findings are early and do not yet show a treatment for people.
-
Type 1 diabetes (T1D) is a serious disease which affects millions of people worldwide and is a major factor for vascular contributions to cognitive impairment and dementia (VCID).
Why it matters
In mice with diabetes, this study found that increased reactive oxygen species from mitochondria in brain artery cells led to DNA damage and vascular dementia in both males and females. The results suggest that targeting this process might help prevent vascular dementia related to diabetes, but this is early animal research and not yet tested in people.
-
The amyloid precursor protein intracellular domain (AICD), a cleavage product of amyloid precursor protein implicated in Alzheimer disease and amyloid lateral sclerosis, is a functionally important but structurally elusive intrinsically disordered protein.
Why it matters
This biophysical study describes how a 35-residue segment of the amyloid precursor protein intracellular domain shifts between compact and extended shapes in laboratory simulations and measurements. It offers structural insights into how this protein fragment might interact with other molecules, but it does not test any treatment, prevention or cure in people or animals.
-
GLP-1 RAs may offer neuroprotective benefits in patients with postoperative delirium and encephalopathies..
Why it matters
This scoping review of animal and clinical studies suggests GLP-1 receptor agonists may offer neuroprotective benefits such as anti-apoptotic, anti-inflammatory and cognitive-enhancing properties in delirium and encephalopathy. The authors note there is limited literature on their benefits in these conditions.
-
Cerebral amyloid angiopathy (CAA) is a common age-related disorder, a prominent comorbidity of Alzheimer disease (AD), and causes vascular cognitive impairment and dementia.
Why it matters
In a transgenic rat model, animals with two copies of the mutated gene developed more severe cerebral amyloid angiopathy type-2 with fibrillar plaques, astrocytic and microglial responses, and phosphorylated tau in surrounding neurites. Their brain proteomes shared many changes with a rat model of Alzheimer's disease, including activated pathways such as transforming growth factor-beta1 signaling.
-
ε4 heterozygous woman with mild cognitive impairment and CSF biomarker evidence of AD underwent treatment with intravenous lecanemab.
Why it matters
In one patient with Alzheimer disease, an incidental cavernous malformation in the brain grew larger on MRI after 13 lecanemab infusions, without new amyloid-related imaging abnormalities, and treatment was stopped. This is a single case report, so it cannot show how often such changes occur or whether lecanemab caused them.
-
Alzheimer’s disease (AD) remains a significant global health challenge with limited FDA-approved treatments, necessitating the search for novel preventive strategies.
Why it matters
In cells and in patients with mild cognitive impairment, pomegranate seed oil showed anti-inflammatory and antioxidant potential and effects on Alzheimer's-related biomarkers. The findings suggest it may serve as an early-stage intervention to delay or mitigate Alzheimer's progression, though the evidence is described as supporting a possible role rather than proven benefit.
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.
- Understanding white matter disease: imaging-pathological correlations in vascular cognitive impairment
- Atypical parkinsonism in Afro-Caribbean and Indian origin immigrants to the UK
- Defective gallium-transferrin binding in Alzheimer disease and Down syndrome: possible mechanism for accumulation of aluminium in brain
- Comparative profiling of cortical gene expression in Alzheimer's disease patients and mouse models demonstrates a link between amyloidosis and neuroinflammation
- Cerebral small vessel disease in memory center patients with dementia with lewy bodies and Alzheimer’s disease
- Effects of alpha-synuclein immunization in a mouse model of Parkinson's disease
- Neurotoxic effects of TDP-43 overexpression in C. elegans
- Synaptic transport of human immunodeficiency virus-Tat protein causes neurotoxicity and gliosis in rat brain
- Reduced frontotemporal functional connectivity in schizophrenia associated with auditory hallucinations
- Prion-Protein-interacting Amyloid-β Oligomers of High Molecular Weight Are Tightly Correlated with Memory Impairment in Multiple Alzheimer Mouse Models