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 5,209 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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Compared with non-PVE-corrected data, PVE-corrected data yielded significantly higher changes in regional and composite SUV ratio (SUVR) over time ( P = 0.0002 for composite SUVRs).
Why it matters
Correcting for partial-volume effects changed longitudinal amyloid PET measurements and suggested the amyloid buildup curve does not plateau at an early symptomatic stage. This is a technical imaging analysis and does not test any treatment, cure or prevention.
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Navigation testing in real space is a promising approach to identify patients with aMCI with underlying Alzheimer pathology.
Why it matters
Among 21 patients with amnestic mild cognitive impairment, those with amyloid in the brain performed worse on real-space navigation tasks than those without amyloid and healthy controls. This suggests navigation testing might help identify which patients with mild cognitive impairment have underlying Alzheimer's disease, but the study was small.
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The search for accessible and cost-effective biomarkers to complement current cerebrospinal fluid (CSF) and imaging biomarkers in the accurate detection of Alzheimer disease (AD) and other common neurodegenerative disorders remains a challenging task.
Why it matters
This review discusses saliva as a potential source of biomarkers for Alzheimer's disease and related disorders, noting practical advantages over other biofluids but also challenges in collecting saliva from elderly people. It does not report any treatment, cure, or prevention of Alzheimer's disease.
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The experimental results demonstrate that the SVM with RBF achieved an encouraging performance with sensitivity (SEN), specificity (SPE), and accuracy (ACC) values of 82.65%, 87.17%, and 84.35%, respectively (AUC = 0.861, 95% CI = 0.820-0.902), for the differential diagnosis between VaD and AD.
Why it matters
This study used structural MRI and machine learning to distinguish vascular dementia from Alzheimer's disease, achieving 84.35% accuracy. It is a diagnostic aid, not a treatment, cure, or prevention for Alzheimer's disease.
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The current study aimed to investigate the effects of group reminiscence therapy on cognitive function, depression, neuropsychiatric symptoms, and activities of daily living in patients with mild-to-moderate Alzheimer disease (AD).
Why it matters
In this trial, group reminiscence therapy improved depressive and neuropsychiatric symptoms in people with mild to moderate Alzheimer disease compared with controls. It addresses symptom management, not curing or preventing the disease.
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The budgetary impacts are not insignificant but are small in comparison to the likely market price of any disease-modifying treatments or to the probable costs of missed or inaccurate diagnosis.
Why it matters
If future Alzheimer's drugs are offered only to people with confirmed amyloid, many more PET scans and spinal-fluid (CSF) tests will be needed. Using a literature review and expert input, this UK analysis estimated that 100,000 extra amyloid PET scans would cost £113 million a year and 100,000 extra CSF tests £48 million a year, with higher costs likely in the first year. The authors judged these costs small next to likely drug prices or the costs of missed diagnosis, but the study gives no figures for those comparisons and tests no treatment.
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In this work, we demonstrate how computational multi-scale brain modeling links phenomena of different scales and therefore identifies potential disease mechanisms leading the way to improved diagnostics and treatment.
Why it matters
This study used computational multi-scale brain modeling to link molecular pathways with large-scale brain dynamics and identify potential disease mechanisms in Alzheimer's disease. It is a proof-of-concept modeling study and does not test any treatment, cure, or prevention in patients.
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46/100
Alzheimer's disease (AD), Parkinson's disease (PD), frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS), Huntington's disease (HD), and prion diseases have a certain degree of clinical, pathological, and molecular overlapping.
Why it matters
In a Thai early-onset Alzheimer's disease cohort, next-generation sequencing of 50 genes found a novel APP p.V604M mutation and the known causative PSEN1 variant. This is a genetic characterization study, so it does not show whether any treatment can prevent or cure the disease.
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Alzheimer's disease (AD) is the leading cause of dementia in the United States and afflicts >5.7 million Americans in 2018.
Why it matters
This review argues that modifiable factors such as lifestyle, air pollution and pesticide exposure, together with non-modifiable factors like age, sex and APOE4, should be combined into personalized prevention and treatment approaches. It is a review of existing data and a suggested framework, not a trial showing that such an approach works.
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Neuroimaging features of early-onset AD in comparison to late-onset AD include greater frequency of hippocampal sparing and posterior neocortical atrophy, increased tau burden, and greater connectomic changes affecting frontoparietal networks rather than the default mode network.
Why it matters
This review describes how early-onset Alzheimer disease differs from late-onset disease, including more genetic predisposition, a more aggressive course, and different brain imaging features. It is descriptive and does not report any treatment, cure, or prevention.
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46/100
Vascular risk factors, sleep disorders, and traumatic brain injury are associated with an increased risk of AD, while increased cognitive and physical activity throughout the lifespan reduce the risk of disease.
Why it matters
This review describes that vascular risk factors, sleep disorders, and traumatic brain injury are associated with increased Alzheimer's disease risk, while increased cognitive and physical activity throughout life reduce risk, and that APOE ε4 is the primary genetic risk factor. It also notes that a comprehensive treatment plan includes symptomatic medications and care for comorbid conditions, and it does not report a cure or prevention.
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AD is characterised by a significant alteration in the circulating levels of the cytokines and receptors of the IL-1 family.
Why it matters
Measuring blood levels of IL-1 family inflammation proteins, this study found several of them increased in Alzheimer's patients, with one receptor increased only in mild cognitive impairment. The authors suggest these could serve as diagnostic markers or therapeutic targets, but this is a marker study and no treatment was tested.
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It has become increasingly evident that neuroinflammation plays a critical role in the pathophysiology of Alzheimer's disease (AD) and other neurodegenerative disorders.
Why it matters
This review discusses imaging of neuroinflammation in Alzheimer's disease and notes that many immune-related genes are linked to increased risk. It is about detection methods and does not report a treatment, cure, or prevention.
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We found a general trend of increased degree of asymmetry with increasing severity of diagnosis.
Why it matters
This imaging study found that asymmetry between the left and right hippocampus increased with severity of diagnosis from healthy controls through mild cognitive impairment to Alzheimer's disease, and greater asymmetry in one subfield correlated with worse learning scores in Alzheimer's patients. These findings describe a possible marker of disease severity but do not test any treatment or show a way to prevent or cure the disease.
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SIs on the LASSI-L related to PSI and frPSI uniquely differentiated Amy+ and Amy- participants with aMCI and likely reflect deficits with inhibition and source memory in preclinical AD not captured by traditional cognitive measures.
Why it matters
This study found that semantic intrusion errors on memory testing distinguished people with amnestic mild cognitive impairment who were amyloid positive from those who were amyloid negative or had other brain disorders. It is a diagnostic study and does not report any treatment, cure, or prevention of Alzheimer's disease.
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The classical amyloid cascade model for Alzheimer's disease (AD) has been challenged by several findings.
Why it matters
This paper proposes a model in which Alzheimer's disease may originate in the periphery, involving APOE ε4, altered miRNA expression, and epigenetic dysregulation of TREM2. It is a proposed model and does not test any treatment, cure, or prevention.
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46/100
Our findings imply that the current version of the Boston criteria may not be sufficient enough to remove non-CAA cases from a cognitively impaired population, especially in the absence of cSS.
Why it matters
Among patients with probable cerebral amyloid angiopathy, those with cortical superficial siderosis had more Alzheimer-like brain atrophy and lower hippocampal volume, and all amyloid-negative cases were in the group without siderosis. This is about imaging patterns and diagnosis, not about treating, curing, or preventing Alzheimer's disease.
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Disorders associated with early-life alterations in amyloid precursor protein production or processing are associated with a distinct pattern of early striatal fibrillary Aβ deposition before significant cognitive impairment.
Why it matters
Using Pittsburgh Compound B-positron emission tomography in 23 people with Down syndrome, 10 with preclinical autosomal dominant Alzheimer's disease, 17 with late-onset Alzheimer's disease and 16 with preclinical Alzheimer's disease, the study found that Down syndrome and preclinical autosomal dominant Alzheimer's disease shared increased bilateral striatal and thalamic amyloid-beta deposition compared with the other groups. The authors suggest this distinct pattern could point to targets for early intervention.
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ADAM10 is a metalloproteinase acting on the amyloid precursor protein (APP) as an alpha-secretase in neurons.
Why it matters
Screening a library of FDA-approved drugs, researchers found that disulfiram, a medicine used for alcohol dependence, boosted ADAM10, an enzyme that steers the amyloid precursor protein away from forming amyloid-beta. In human nerve cells it raised ADAM10 and protective sAPP-alpha, and in Alzheimer model mice it reduced plaque in part of the hippocampus and eased behavioral problems. The authors suggest disulfiram could be repurposed for Alzheimer's, but say its efficacy and safety still have to be tested in Alzheimer patients.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the main cause of dementia among the elderly worldwide.
Why it matters
This review describes noncoding RNAs as being involved in the onset and development of Alzheimer's disease and as possible biomarkers and therapeutic targets. It states that no effective therapies are available yet, so this is background research rather than a treatment.
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The blood-brain barrier (BBB) is involved in the pathogenesis of Alzheimer's disease (AD).
Why it matters
This review states that blood-brain barrier dysfunction causes failure of amyloid-β transport out of the brain, with decreased LRP-1 and increased RAGE at the barrier contributing to this failure. It describes a mechanism and does not show that repairing the barrier treats or prevents Alzheimer's disease.
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Alzheimer's disease (AD) is the most prevalent form of dementia.
Why it matters
This review discusses phytochemicals as possible inhibitors of the NF-κB inflammatory pathway, which is proposed as a target for inflammation-based Alzheimer's therapy. It does not report results from a clinical trial, so it cannot yet show whether these compounds treat or prevent Alzheimer's disease in people.
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This technique could be applied to questions in social gerontology related to how social media outlets reflect and shape attitudes bearing on other developmental outcomes.
Why it matters
This study analyzed Twitter posts and found that about 21% of Alzheimer's-related tweets used the disease keywords in ways that perpetuate public stigma. It addresses social attitudes and stigma, not the treatment, cure or prevention of Alzheimer's disease.
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Astrocytes have essential roles in the central nervous system and are also implicated in the pathogenesis of neurodegenerative disease.
Why it matters
This review describes astrocytes as complex, heterogeneous cells implicated in the pathogenesis of neurodegenerative disease, and notes that no single label captures the entire astrocyte population. It offers no treatment, cure or prevention findings.
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Alzheimer's disease (AD) is the most common type of dementia among individuals 65 or older.
Why it matters
This review discusses the intersection of genetics and social determinants of health in Alzheimer's disease within the Latino community. It does not test any treatment, cure, or prevention for Alzheimer's disease.
From across this topic
10 of the 5,172 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.
- Gut microbiome alterations in Alzheimer's disease
- Decreased phospholipase A2 activity in Alzheimer brains
- β-Amyloid PET Signal Reduction in Prior ARIA-E Regions after Antiamyloid Therapy for Alzheimer Disease
- Trajectories of the Hippocampal Subfields Atrophy in the Alzheimer's Disease: A Structural Imaging Study
- Neuroinflammation in the pathogenesis of Alzheimer's disease. A rational framework for the search of novel therapeutic approaches
- Both Amyloid and Tau Assessments Are Desired Before Initiating Disease-modifying Therapy for Alzheimer Disease: Three Real-world Cases
- Disentangling the Causal Effects of Education and Participation Bias on Alzheimer Disease Using Mendelian Randomization
- Plasma Glial Fibrillary Acidic Protein in the Alzheimer Disease Continuum: Relationship to Other Biomarkers, Differential Diagnosis, and Prediction of Clinical Progression
- Multi-scale 3D CNN with imbalance-aware training for structural MRI-based six-class Alzheimer disease staging
- Biomarkers for dementia and mild cognitive impairment in Parkinson's disease