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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This article describes the public health impact of Alzheimer's disease (AD), including incidence and prevalence, mortality and morbidity, use and costs of care, and the overall impact on family caregivers, the dementia workforce and society.
Why it matters
This 2022 report describes the public health burden of Alzheimer's. It says there are fewer family caregivers than a decade earlier, each one provides more care, and caregivers face an increased risk of emotional distress and poorer mental and physical health, which the report says COVID-19 made worse. A survey commissioned by the Alzheimer's Association found barriers to public understanding of mild cognitive impairment, and the report calls for better awareness and diagnosis, especially in underserved communities. The page gives no figures and tests no treatment, so it describes the problem rather than showing what reduces it.
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Many drugs that target amyloid-β (Aβ) in Alzheimer disease (AD) have failed to demonstrate clinical efficacy.
Why it matters
This review discusses four anti-amyloid antibodies that remove amyloid plaque, including aducanumab, which received accelerated approval using plaque reduction as a surrogate endpoint. It notes that the rationale for approval and the extent of clinical benefit are under intense debate, so it does not establish a cure or clear clinical benefit.
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Plasma-based biomarkers would be potential biomarkers for early diagnosis of Alzheimer's disease (AD) because they are more available and cost-effective than cerebrospinal fluid (CSF) or neuroimaging.
Why it matters
This study evaluated whether plasma p-tau181 could predict neurodegeneration and progression to Alzheimer's dementia in ADNI participants across cognitive stages. It is about a blood-based predictor, not a treatment, cure, or prevention.
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The results were validated in an independent sample of 610 patients with Parkinson's disease from the National Institute of Neurological Disorders and Stroke Parkinson's Disease Biomarker Program (PDBP).
Why it matters
This study used machine learning to identify Parkinson's disease states and model progression, validated in 610 patients, with those starting in one state having the shortest time to a terminal state. This concerns Parkinson's disease progression and does not address treating, curing or preventing Alzheimer's disease.
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This study examines whether neuroticism is differentially associated with risk of incident Alzheimer's disease (AD), vascular dementia (VD), and frontotemporal dementia (FTD) using a prospective study design.
Why it matters
This study examined whether the personality trait neuroticism is linked to different types of dementia, including Alzheimer's disease, vascular dementia, and frontotemporal dementia. It does not show that changing personality or treating neuroticism prevents or cures dementia.
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This article describes the public health impact of Alzheimer's disease (AD), including incidence and prevalence, mortality and morbidity, use and costs of care, and the overall impact on caregivers and society.
Why it matters
This report describes the public health impact of Alzheimer's and notes that racial and ethnic minorities have a higher burden of illness and less access to care. It emphasizes the need for more diversity in care and research, but does not test any treatment or prevention.
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Further studies are needed to determine whether COVID-19 may lead to an increased risk of developing NDD in susceptible individuals.
Why it matters
This review of published studies reports that people with dementia, including Alzheimer's disease, are at higher risk of hospitalisation and death from COVID-19, while those with Parkinson's disease are not. The authors urge extra precautions to prevent infection and manage other health conditions in people with Alzheimer's, and say more research is needed on whether COVID-19 could raise the risk of developing neurodegenerative disease.
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AD patients with ELA expressed significantly greater levels of APOE than ALA APOE ε4 carriers.
Why it matters
This single-nucleus RNA sequencing study found that Alzheimer disease patients with European local ancestry expressed more APOE than those with African local ancestry. The authors suggest these expression differences could contribute to the reduced risk seen in African APOE ε4 carriers, but this is a preliminary finding needing further study.
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Lowering brain Aβ must be accomplished early in the evolution of AD.
Why it matters
Using amyloid PET scans followed for up to 9 years, this study found that the transition from amyloid negative to positive took about 6.4 years and another 13.9 years to the onset of mild cognitive impairment, with deposition rates slowing only 3.8 years after reaching positivity. The authors conclude that lowering brain amyloid must be done early in the disease process, but this observational study does not itself test a treatment.
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Alzheimer's disease is a progressive, irreversible neurodegenerative disease impacting cognition, function, and behavior.
Why it matters
This review states that detecting early-stage Alzheimer's disease in clinical practice is challenging, with barriers including limited clinician time and symptoms being dismissed as normal aging. It argues that early and accurate detection is fundamental for screening, diagnosis and management, and lets patients and caregivers plan ahead and make lifestyle changes that could help maintain quality of life for longer.
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Alzheimer disease (AD) is the most common form of neurodegenerative disease, estimated to contribute 60-70% of all cases of dementia worldwide.
Why it matters
This 2021 review argues that the amyloid cascade hypothesis, which holds that amyloid-β build-up in the brain is the starting event, is "insufficient to explain many aspects" of Alzheimer's. It says raised inflammatory markers in patients and risk genes tied to innate immunity "suggest" that brain inflammation plays a prominent role, and it looks at how inflammation interacts with amyloid and tau, focusing on microglia, the brain's immune cells. It is a review of existing evidence, not a new study, and reports no treatment, cure or prevention.
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& objective Evidence is limited on how estimated glomerular filtration rate (eGFR) and urinary albumin-creatinine ratio (UACR) relate to dementia at different ages.
Why it matters
This ARIC Study analysis evaluated estimated glomerular filtration rate and urinary albumin-creatinine ratio in midlife and older age as risk factors for dementia. It is observational, so it cannot prove that treating kidney disease would prevent dementia.
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Currently established and employed biomarkers of Alzheimer's disease (AD) predominantly mirror AD-associated molecular and structural brain changes.
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Most approaches to machine learning from electronic health data can only predict a single endpoint.
Why it matters
This study used an unsupervised machine learning model to simulate 18-month patient trajectories from 1909 patients with mild cognitive impairment or Alzheimer's disease. The model predicted changes in total ADAS-Cog scores with the same accuracy as specifically trained supervised models, which may help personalized forecasting of disease progression.
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The cerebrospinal fluid (CSF) biochemical markers (biomarkers) Amyloidβ 42 (Aβ 42 ), total Tau (T-tau) and Tau phosphorylated at threonine 181 (P-tau 181 ) have proven diagnostic accuracy for mild cognitive impairment and dementia due to Alzheimer's Disease (AD).
Why it matters
This review concludes that the cerebrospinal fluid Aβ42/40 ratio, rather than the absolute value of Aβ42, should be used when analysing CSF Alzheimer's disease biomarkers to improve the percentage of appropriately diagnosed patients. It concerns improving diagnostic accuracy and distinguishing Alzheimer's disease from other dementias, not treating, curing or preventing the disease.
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Alzheimer disease (AD) is a major cause of age-related dementia.
Why it matters
This review pulls together research suggesting that in Alzheimer's disease and amnestic mild cognitive impairment, the brain's use of glucose is "dramatically decreased", which the authors say is "probably owing, at least in part" to oxidative damage to the enzymes that make energy (ATP). They describe a proposed chain in which less energy weakens synapses and kills neurons, leading to thinning of key brain areas. It is a summary of existing work, not a new study: it reports no patient data and no tested treatment, and the drug ideas it raises are only "potential" ways to slow the disease.
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Nearly half of all adults older than 60 years of age report sleep disturbance, as characterised either by reports of insomnia complaints with daytime consequences, dissatisfaction with sleep quality or quantity, or the diagnosis of insomnia disorder.
Why it matters
This review proposes that sleep disturbance contributes to cognitive decline and might increase the risk of Alzheimer's disease dementia by increasing β-amyloid burden, and that the relationship between sleep and Alzheimer's disease may be bidirectional. It suggests that both sleep disturbance and inflammatory activation might be modifiable risk factors, which could help identify targets for prevention.
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Early Life Stress (ELS) rodent models have successfully demonstrated sequelae of maternal separation resulting in LOAD-analogous pathology, thereby supporting a role of insulin receptor signalling pertaining to GSK-3beta facilitated tau hyper-phosphorylation and amyloidogenic processing.
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PET can evaluate amyloid expansion from cortex to subcortex.
Why it matters
Not everyone with a lot of amyloid in the brain's outer layer (cortex) declines quickly. This study of 1,433 people (646 cognitively normal, 574 with mild cognitive impairment, 213 with Alzheimer's) found on 3-year follow-up PET scans that amyloid showed up first in the cortex and later in a deeper region, the striatum. A three-stage scheme that also counted striatal amyloid predicted hippocampal volume and later cognition better than a three-stage scheme based on cortex alone. The authors say this "may increase predictive power in Alzheimer's dementia research"; it is not a clinical test.
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The blood-brain barrier (BBB) keeps neurotoxic plasma-derived components, cells, and pathogens out of the brain.
Why it matters
This review discusses evidence that blood-brain barrier breakdown and dysfunction occur early in Alzheimer's disease, before dementia and neurodegeneration, and examines this in animal models. It states the role of blood-brain barrier breakdown is still not fully understood and comments on future approaches as a basis for developing new therapies.
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See Derry and Kent (doi:10.1093/awx167) for a scientific commentary on this article.
Why it matters
Among people with amyloid in the brain, higher levels of iron in the hippocampus, measured by a special MRI method, predicted faster cognitive decline. This suggests iron may combine with amyloid to speed progression, but it does not show that reducing iron helps patients.
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This study tested the hypotheses that late-midlife obstructive sleep apnea (OSA) and short and long sleep duration are associated with dementia over 15 years of follow-up.
Why it matters
This study found that obstructive sleep apnea and sleep duration were not associated with risk of incident dementia. It is an observational study, and it did not find a significant link.
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Plasma BACE1 activity is significantly increased in MCI converters and patients with probable AD.
Why it matters
In this study, plasma BACE1 activity was higher in people with mild cognitive impairment and probable Alzheimer's disease than in healthy controls, and those with mild cognitive impairment who converted to Alzheimer's dementia had significantly higher BACE1 activity. This suggests a possible blood-based marker for predicting conversion, but no treatment was tested.
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Our PET study replicated postmortem spreading patterns of tau and amyloid-β pathologies.
Why it matters
In 195 people ranging from healthy to Alzheimer's dementia, each scanned once for tau and amyloid, this PET study inferred that tau appears first in the medial temporal lobe and spreads stepwise outward, reaching the primary cortex last. Amyloid ran almost the other way: it appeared across the neocortex first and reached the medial temporal regions last, which the authors say replicates patterns seen at autopsy. The resulting image-based tau stage correlated with general cognitive status, and cortical thinning showed up only in the most advanced stages (V and VI). This is an association from one-time scans, not a tested diagnostic tool or treatment finding.
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Reduced AV-1451 binding in neuritic pathology compared to neurofibrillary tangles suggests that the maturity of tau pathology may affect AV-1451 binding and suggests complexity in AV-1451 binding.
Why it matters
In autopsy brain tissue from 38 people with Alzheimer's and other dementias, the tau PET tracer AV-1451 bound strongly to the tau tangles of Alzheimer's but weakly to tau in diseases with only one tau type (3R or 4R, such as Pick disease), minimally to TDP-43 regions, and not at all to α-synuclein. It also showed "off-target" binding in blood vessels, iron-rich areas, the substantia nigra, choroid plexus calcifications and meningeal melanin. The authors conclude that the tracer has "limited clinical utility" for 3R-only or 4R-only tau diseases, does not fully track early-stage tau spread in Alzheimer's, and that clinical use "will require a familiarity" with its off-target binding.
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.
- The Diagnostic Role of FDG-PET in Dementias Presenting with Language and Behavioral Symptom
- Decreased drebrin mRNA expression in Alzheimer disease: correlation with tau pathology
- NOVEL DRUG DELIVERY SYSTEM: A PANDORA BOX FOR THE MANAGE MENT OF ALZHEIMER NOVEL DRUG DELIVERY IN ALZHEIMER
- Neurodegenerative disorders: A Holistic study of the explainable artificial intelligence applications
- Comparison of different MRI brain atrophy rate measures with clinical disease progression in AD
- Effects of rivastigmine transdermal patch and capsule on aspects of clinical global impression of change in Alzheimer's disease: a retrospective analysis
- Biomarker Modeling of Alzheimer’s Disease
- Immunoassay detection of multiphosphorylated tau proteoforms as cerebrospinal fluid and plasma Alzheimer's disease biomarkers
- Long-term surveillance of the anti-amyloid monoclonal antibody lecanemab: rights and duties of pharmacovigilance
- Validity and reliability of the Alzheimer's Disease Cooperative Study-Clinical Global Impression of Change. The Alzheimer's Disease Cooperative Study