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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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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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.
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Mild Alzheimer's disease is the leading cause of dementia, accounting for 50-70% of cases.
Why it matters
This overview states that Alzheimer's disease is a complex and multifactorial disorder determined by genetic susceptibility and environmental factors across the life course, and that epidemiological studies have identified potential modifiable risk and protective factors. It highlights the concept of early prevention, noting that interventions targeting several risk factors in non-demented elderly or even middle-aged people might prevent or delay onset, but reports no cure.
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Aging and the emergence of age-associated illnesses are one of the major challenges of our present society.
Why it matters
This systematic review examined whether three food-derived substances, epigallocatechin gallate, fisetin and spermidine, help with three hallmarks of Alzheimer's: autophagy (the cell's clean-up system), neuroinflammation and cell ageing (senescence). The authors conclude the evidence gives a positive outlook for these substances as a possible new treatment option, perhaps combined with other preventive measures. They present them as candidates for a multi-layered approach, not as established therapies.
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Apolipoprotein E (ApoE) is of great interest due to its role as a cholesterol/lipid transporter in the central nervous system (CNS) and as the most influential genetic risk factor for Alzheimer disease (AD).
Why it matters
This review summarizes what is known about the structure of apolipoprotein E and how it relates to Alzheimer disease biology. It identifies areas for future study but reports no treatment, cure, or prevention findings.
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Cross-sectional data, including CSF analytes, molecular imaging of cerebral fibrillar β-amyloid (Aβ) with PET using the [ 11 C] benzothiazole tracer Pittsburgh compound B (PiB), MRI-based brain structures, and clinical/cognitive outcomes harmonized from 8 studies, collectively involving 3,284 cognitively normal individuals 18 to 101 years of age, were analyzed.
Why it matters
This study estimated the order in which Alzheimer's disease biomarkers change in cognitively normal adults by analyzing data from eight studies. It is a cross-sectional observational study and does not test any treatment, cure, or prevention.
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The results of this review will determine the efficacy and safety of herbal medicine for AD.
Why it matters
This is a protocol for a planned systematic review and meta-analysis of herbal medicine for Alzheimer's disease, so it reports no results yet. It states only that the review will determine the efficacy and safety of herbal medicine, meaning no conclusion about treatment is available.
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We observed good convergence among the 4 Good convergence was obtained among several methods for determining an optimal cutoff for 18 F-AZD4694 PET positivity.
Why it matters
This study found that a threshold of 1.55 SUVR for 18F-AZD4694 PET reliably distinguished amyloid positivity, with good agreement across methods. This is about how to read a scan, not about treating, curing, or preventing Alzheimer's disease.
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Alzheimer's disease (AD) is the most common neurodegenerative disorder seen in age-dependent dementia.
Why it matters
This review describes evidence for roles of amyloid beta, tau, and glial dysfunction in Alzheimer's disease and notes that there is currently no effective treatment. It discusses possible contributing factors such as genetics, aging, environment, lifestyle, APOE, infection, sleep, and microbiota, but reports no treatment, cure, or prevention.
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Thirty-three percent of LLD participants met ADNI criteria for mild cognitive impairment.
Why it matters
In 119 older adults with late-life depression compared with 119 nondepressed participants, the depressed group had less global amyloid beta accumulation. Thirty-three percent of the depressed participants met criteria for mild cognitive impairment, suggesting that amyloid may not be the main driver of memory problems in late-life depression.
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.
- Neuroticism, conscientiousness, and in vivo Alzheimer pathologies measured by amyloid PET and MRI
- High Cortisol and the Risk of Dementia and Alzheimer's Disease: A Review of the Literature
- Neuroinflammation in Alzheimer's disease
- Review: systemic inflammation and Alzheimer's disease
- 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