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 5,413 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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Neuronal dysfunction and cognitive deterioration in Alzheimer's disease (AD) are likely caused by multiple pathophysiological factors.
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ARIA monitoring is important to inform treatment dosing decisions and might be improved through assistive software.
Why it matters
This diagnostic study assessed an artificial intelligence-based software tool for assisting radiological interpretation of brain MRI scans in patients monitored for amyloid-related imaging abnormalities (ARIA). It addresses monitoring of a treatment side effect, not treating, curing or preventing Alzheimer's disease itself.
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For amyloid positive individuals Aβ42/Aβ40, glial fibrillary acidic protein and p-tau181 were the top predictors of cognitive decline while Aβ42/Aβ40 was prominent for amyloid negative participants across all age groups.
Why it matters
This study tested whether combining Alzheimer's plasma biomarkers with MRI, cardiovascular, genetic, and lifestyle measures improves prediction of cognition. It concerns prediction, not treating, curing, or preventing Alzheimer's disease.
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According to the World Health Organization (WHO), dementia is the seventh leading reason of death among all illnesses and one of the leading causes of disability among the world's elderly people.
Why it matters
This study combined clinical, MRI, and psychological data with machine learning to classify five categories including Alzheimer's disease, reporting 98.81% accuracy with a Random Forest classifier. It is about improving diagnosis, not about treating, curing, or preventing Alzheimer's disease.
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Recent studies show that Alzheimer's disease (AD) has many common links with conditions associated with insulin resistance, including neuroinflammation, impaired insulin signaling, oxidative stress, mitochondrial dysfunction and metabolic syndrome.
Why it matters
This review looks at diabetes drugs as possible Alzheimer's treatments, since the two conditions share problems such as insulin resistance and inflammation. Metformin, intranasal insulin, thiazolidinediones and incretins showed positive effects in both people and animal models, but rosiglitazone may carry a significant risk of side effects. Clinical results for metformin in Alzheimer's were limited and contradictory, so the case is not settled.
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Evidence shows that ADAM10 levels are altered in platelets, plasma, serum, and CSF of individuals with AD.
Why it matters
This systematic review of 17 studies looked at ADAM10, an enzyme that steers amyloid precursor protein away from making amyloid-β, as a possible Alzheimer's biomarker. ADAM10 was consistently lower in platelets but higher in plasma of people with Alzheimer's, while spinal fluid results conflicted, possibly due to differing lab methods. The authors see it as a possible complementary biomarker but say cut-off values still need to be established.
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53/100
A location dynamics model and ADRD-focused future directions are offered for guiding rural practitioners, researchers, and policymakers in mitigating rural disparities.
Why it matters
This review reports that people in rural communities face heightened risk and burden from Alzheimer's disease and related dementias, and identifies individual, interpersonal and community factors. It offers a location dynamics model and future directions for reducing these disparities, rather than testing a treatment.
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White matter hyperintensities (WMH) correlate with Alzheimer disease (AD) biomarkers cross-sectionally and modulate AD pathogenesis.
Why it matters
This longitudinal study examined how white matter hyperintensities relate over time to established Alzheimer disease biomarkers, including cerebrospinal fluid amyloid and tau measures, PET amyloid imaging, hippocampal volume and cortical thickness, across the adult life span. It describes relationships between markers and does not test any treatment or prevention.
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Altered levels of kynurenines in blood and cerebrospinal fluid (CSF) have been reported in Alzheimer's disease (AD).
Why it matters
This study measured kynurenines in plasma and CSF and checked how they relate to Alzheimer's amyloid and tau markers across the cognitive spectrum. It explores possible biological pathways but does not test a treatment or prevention.
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Plasma GFAP effectively distinguished AD dementia from multiple neurodegenerative diseases, gradually increased across the AD continuum, predicted the individual risk of AD progression, and strongly correlated with AD CSF/neuroimaging biomarkers.
Why it matters
In this study, plasma GFAP was higher in Alzheimer's disease than in non-Alzheimer's dementia and non-demented individuals, and higher levels predicted risk of Alzheimer's progression and cognitive decline. It is about diagnosis and prediction, not about treating, curing or preventing the disease.
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The AD drug development pipeline is advancing agents directed at a variety of target processes.
Why it matters
This report found that as of January 1, 2023, there were 187 trials assessing 141 unique treatments for Alzheimer's disease, with disease-modifying therapies the most common. It describes the current drug development pipeline and the number of participants needed, but reports no results on whether any treatment works.
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53/100
Alzheimer's disease is one of the most commonly diagnosed cases of senile dementia in the world.
Why it matters
This review discusses inflammation as one factor in Alzheimer's disease and suggests that understanding it better may aid early diagnosis and new treatment strategies. It reports no tested treatment or cure and notes that many aspects of the inflammatory process remain unexplained.
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This article describes the public health impact of Alzheimer's disease, including prevalence and incidence, mortality and morbidity, use and costs of care, and the overall impact on family caregivers, the dementia workforce and society.
Why it matters
This report describes the public health impact of Alzheimer's, including costs and effects on family caregivers. It does not test any treatment or prevention, so it does not directly change how the disease is treated or cured.
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Both FC-BAG and S-BAG are elevated in CI participants.
Why it matters
Brain age gap estimates were elevated in cognitively impaired participants, and in those participants elevated structural and multimodal estimates were associated with more advanced Alzheimer disease pathology and lower cognitive performance. This is a cross-sectional observational study of brain age estimates, not a treatment, cure or prevention for Alzheimer's disease.
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Higher soluble plasma p-tau levels may be the result of an intersection between insoluble deposits of amyloid-β and tau accumulation in brain, and may be associated with locus coeruleus degeneration.
Why it matters
In 35 autopsied participants, higher plasma levels of phosphorylated tau were most strongly linked to tau burden in the parietal cortex, and a lower count of locus coeruleus neurons was linked to higher plasma p-tau. This helps explain what blood p-tau measures but does not test any treatment, cure or prevention.
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The combination of amyloid and tau PETs was associated with changes in management and diagnosis of MCI and dementia, and the second-generation tau PET has a strong impact on the changes in diagnosis and management in memory clinics.
Why it matters
In 126 memory clinic participants, combining amyloid and tau PET scans changed the suspected cause of symptoms in many patients and changed management for about half of those with mild cognitive impairment. Tau PET was more strongly linked to changes in management than amyloid PET.
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53/100
Microglia are strongly implicated in the development and progression of Alzheimer's disease (AD), yet their impact on pathology and lifespan remains unclear.
Why it matters
In mice engineered to lack microglia, amyloid plaques shifted to cerebral amyloid angiopathy with bleeding, calcification and early death, and injecting normal microglia prevented these problems. These are mouse results and do not establish a treatment, cure or prevention for people.
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Higher grey matter volumes/cortical thickness and fluorodeoxyglucose uptake have been consistently found in cognitively unimpaired individuals with abnormal Alzheimer's disease biomarkers compared with those with normal biomarkers.
Why it matters
In cognitively unimpaired individuals, higher grey matter volumes and cortical thickness and higher fluorodeoxyglucose uptake have been consistently found in those with abnormal Alzheimer's disease biomarkers compared with those with normal biomarkers, possibly linked to neuroinflammatory mechanisms. The study found that tau pathology accompanied by the astrocytic marker YKL-40 was associated with higher grey matter volumes and fluorodeoxyglucose uptake in extensive brain areas, but this is an observational finding and does not establish a treatment, cure, or prevention.
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Higher sNfL concentrations were associated with worse performance in cognitive tests at baseline, including CERAD (B = −10.084, SE = 2.999, p < 0.001) and MMSE (B = −3.014, SE = 1.293, p = 0.021).
Why it matters
In this study, higher serum NfL levels were linked to worse cognitive test scores and predicted more cognitive decline over about 22 months, but not changes in neuropsychiatric symptoms or brain volumes. This marker may help track short-term cognitive worsening, but the study does not show any treatment, cure, or prevention.
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Alzheimer's disease (AD) is the leading cause of dementia in older adults.
Why it matters
This study used several machine learning classifiers on imaging data to predict early-stage Alzheimer's disease, with the best validation average accuracy of 83%. It is a prediction study and does not test any treatment, cure or prevention.
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53/100
To explore markers for synaptic function and Alzheimer disease (AD) pathology in late life depression (LLD), predementia AD and normal controls (NC).
Why it matters
This cross-sectional study compared cerebrospinal fluid markers of synaptic function and Alzheimer-type changes among people with late life depression, predementia Alzheimer disease and normal controls. It examines marker patterns only and provides no evidence about treating, curing or preventing the disease.
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Cerebral white matter lesions (WML) encompass axonal loss and demyelination and are assumed to be associated with small vessel disease (SVD)-related ischaemia.
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Neither fibrillar nor nonfibrillar Aβ content alone sufficed to explain the Aβ PET findings in either AD model.
Why it matters
In mouse models, the amyloid PET signal came from both fibrillar and nonfibrillar amyloid plaque components, not fibrillar amyloid alone. This is animal imaging research and does not show any treatment, cure, or prevention for people.
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Beta-amyloid (Aβ 1-42 ) triggers the phosphorylation of tau protein in Alzheimer's disease (AD), but the relationship between phosphorylated tau (p-tau) and Aβ 1-42 in the blood is not elucidated.
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Alzheimer's disease (AD) is a devastating condition with no effective treatments, with promising findings in rodents failing to translate into successful therapies for patients.
Why it matters
Rhesus monkeys injected with a virus expressing a double tau mutation showed evidence of misfolded tau spreading within 3 months. This is an animal model of Alzheimer's pathogenesis and does not report a treatment, cure, or prevention.
From across this topic
10 of the 5,374 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.
- Neuropathology of nondemented aging: Presumptive evidence for preclinical Alzheimer disease
- Differential neurocognitive network perturbation in amnestic and aphasic Alzheimer disease
- Disrupted Network Topology in Patients with Stable and Progressive Mild Cognitive Impairment and Alzheimer's Disease
- Biomarker-based prediction of progression in MCI: Comparison of AD signature and hippocampal volume with spinal fluid amyloid-β and tau
- Impact of C-Reactive Protein on Cognition and Alzheimer Disease Biomarkers in Homozygous APOE ɛ4 Carriers
- Non-steroidal anti-inflammatory drugs as a treatment for Alzheimer's disease: a systematic review and meta-analysis of treatment effect
- Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models
- Exploring the Pathogenesis of Alzheimer Disease in Basal Forebrain Cholinergic Neurons and Converging Insights from Alternative Hypothesis
- Brain Aging in African-Americans: The Atherosclerosis Risk in Communities (ARIC) Experience
- Plasma multianalyte profiling in mild cognitive impairment and Alzheimer disease