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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Future research should examine whether minimizing drawbacks at the pre-imaging stage has adverse consequences on results disclosure.
Why it matters
Interviews with 59 people with mild cognitive impairment and their care partners found that most wanted amyloid PET results mainly to understand prognosis or for knowledge, and few mentioned possible drawbacks. This concerns how people weigh testing decisions and does not treat, cure or prevent Alzheimer's disease.
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Inclusion criteria included clinical diagnosis of PPA; availability of complete speech, language, and cognitive testing; magnetic resonance imaging performed within 6 months of the cognitive evaluation; and PET carbon 11-labeled Pittsburgh Compound-B or florbetapir F 18 brain scan results.
Why it matters
This study found that most patients with semantic variant and nonfluent/agrammatic variant primary progressive aphasia had negative amyloid PET scans, while most with logopenic variant had positive scans. It concerns diagnosis of primary progressive aphasia variants and does not test any treatment, cure or prevention.
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Serum NfL concentration is increased in FAD prior to symptom onset and correlates with measures of disease stage and severity.
Why it matters
In people with familial Alzheimer's disease mutations, serum neurofilament light was higher in both symptomatic and presymptomatic carriers and correlated with disease stage and severity. This marker may help detect early neurodegeneration, but it is not a treatment, cure, or prevention.
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The utility of plasma total tau level as a prognostic marker for cognitive decline and dementia is not well understood.
Why it matters
This cohort study of 458 participants examined whether plasma total tau level is linked to cognitive decline and risk of mild cognitive impairment or dementia. It is a prognostic marker study and does not test any treatment, cure, or prevention.
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These studies fundamentally deepen our understanding of AD progression and its underlying genetic basis, which in turn informs and improves clinical trial design.
Why it matters
This review of Alzheimer's Disease Neuroimaging Initiative publications reports that structural and functional brain changes can be detected before hippocampal atrophy, that amyloid biomarkers become abnormal first, and that cognitive decline tracks more closely with tau than with amyloid. It also notes that cerebrovascular risk factors may interact with amyloid to worsen white-matter abnormalities, and that these findings are being used to improve clinical trial design.
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See Coulthard and Knight (doi:10.1093/aww335) for a scientific commentary on this article.
Why it matters
This study notes that individuals with mild cognitive impairment and Alzheimer's disease clinical diagnoses can display significant phenotypic heterogeneity. No treatment, cure or prevention effect is reported in the available text.
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Plasma amyloid-β (Aβ) levels are increasingly studied as a potential, accessible marker of cognitive impairment and dementia.
Why it matters
This study examined whether blood levels of amyloid-beta relate to cerebral small vessel disease and cognition in 1201 people before dementia symptoms appear. It is an observational analysis, so it cannot show that measuring or changing these blood levels prevents or treats Alzheimer's disease.
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Periodontitis is common in the elderly and may become more common in Alzheimer's disease because of a reduced ability to take care of oral hygiene as the disease progresses.
Why it matters
In this six-month study of 60 people with mild to moderate Alzheimer's disease, periodontitis at the start was linked to a faster rate of cognitive decline. This is a small observational study and does not show that treating gum disease slows Alzheimer's disease.
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The primary outcome of this trial was negative.
Why it matters
In this small 4-week trial, bexarotene did not change brain amyloid when all patients were analyzed together, though a reduction was seen in ApoE4 noncarriers but not in ApoE4 carriers. This was a proof-of-concept study in only 20 patients, so it does not establish any benefit for treating or preventing Alzheimer's disease.
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Disclosure of pleiotropic information did not increase anxiety or depression and may have decreased distress among persons at increased risk for 2 conditions.
Why it matters
This trial found that disclosing genetic risk information about both Alzheimer's disease and coronary artery disease did not increase anxiety or depression compared with disclosing Alzheimer's risk alone. This concerns how genetic risk information is shared, not treating, curing, or preventing Alzheimer's disease.
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Atrial fibrillation (AF) has been suggested as a risk factor for dementia since it may lead to chronic cerebral hypoperfusion and stroke.
Why it matters
This study examined whether atrial fibrillation, a heart rhythm problem, is linked to developing dementia over 20 years in 6,514 dementia-free participants. If atrial fibrillation raises dementia risk, treating it could be a prevention strategy, but this study only assessed the association.
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Black decedents with AD dementia are more likely to have mixed brain pathologies compared with age-, sex-, education-, and cognition-matched white decedents with AD dementia.
Why it matters
In 122 people with Alzheimer dementia examined after death, Alzheimer brain changes were confirmed in more than 93% of both black and white decedents, but black decedents were less likely to have Alzheimer changes alone (19.5% vs 42.0%) and more likely to have them mixed with other pathology (70.7% vs 50.6%), particularly Lewy bodies and infarcts. Black decedents (n = 41) were matched to white decedents (n = 81) on age at death, sex, education and cognition near death, and also had more severe small- and large-vessel disease. This is an association in a small autopsy group; the study does not say why the difference exists.
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Reference region selection has an important influence on the detection of florbetapir change.
Why it matters
Amyloid PET scans are scored by comparing brain signal against a "reference" area, and in 520 ADNI participants scanned two years apart, the six reference areas tested gave "poor agreement" on how much amyloid had changed. Using people expected to stay stable (n = 14) or to increase (n = 91) as checks, the authors found that areas including white matter gave change measurements that were "more accurate" than cerebellum or pons alone, though they "may result in more conservative estimates of actual change." This is a measurement-methods study for research and trials using one tracer (florbetapir); it does not test any treatment.
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Although the presence of abnormal levels of amyloid-β (Aβ) is associated with higher rates of progression to clinically classified mild cognitive impairment or dementia, little research has evaluated potentially modifiable moderators of Aβ-related cognitive decline, such as anxiety and depressive symptoms.
Why it matters
In people without symptoms who had abnormal amyloid levels, those with more anxiety symptoms declined faster in memory and thinking than those with less anxiety. Since anxiety can be treated, this finding may help identify and manage people at higher risk, though it does not show that treating anxiety prevents Alzheimer's disease.
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Cross-sectional epidemiological and clinical research suggests that lower cardiac index is associated with abnormal brain aging, including smaller brain volumes, increased white matter hyperintensities, and worse cognitive performances.
Why it matters
This study examined whether lower cardiac index is associated with incident dementia and Alzheimer's disease in a cohort of older adults. It is an observational study of a possible risk factor and does not test any treatment, cure, or prevention.
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Observational studies support the use of NSAIDs for prevention of AD, but RCT do not.
Why it matters
In observational studies pooled up to March 2014, people who used NSAIDs had a lower recorded rate of Alzheimer's disease than non-users (relative risk 0.72), and this included both aspirin and non-aspirin NSAIDs; corticosteroids showed no significant link. However, the only randomized trial found "no significant effect" of NSAIDs on Alzheimer's risk in dementia-free people, so the authors conclude that observational studies support NSAIDs for prevention "but RCT do not." They add that the right dose, duration and safety have not been established, so this is not a reason to start taking anti-inflammatory drugs.
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In ADNI, Aβ-positive participants showed more decline than did Aβ-negative participants with regard to the ADCS-PACC score at 24 months (mean [SE] difference, -1.239 [0.522] [95% CI, -2.263 to -0.215]; P = .02).
Why it matters
This study found that a composite cognitive test could detect early decline in people without dementia who had amyloid buildup or carried the APOE epsilon4 allele. It offers a way to measure the first signs of cognitive decline in research, but it does not provide a treatment, cure or prevention for Alzheimer's disease.
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65/100
High Aβ participants were more likely to be APOE ε4+ than low Aβ participants.
Why it matters
Among clinically normal older adults followed for a median of about 1.5 years, those who had both high amyloid and the APOE epsilon4 allele showed the greatest decline in memory. The authors conclude that amyloid and APOE epsilon4 interact to promote short-term decline, but they note that longer follow-up is needed and no treatment or prevention is tested.
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A previous report describes decreased decline in ADAS-cog (delta = 3.1, p = 0.008 at 18 months, ANCOVA with multiple imputation), relative to placebo, following a 5 mg/day dose of TTP488.
Why it matters
This trial tested the drug TTP488 in 399 patients with mild to moderate Alzheimer's disease. It does not report that TTP488 cures or prevents Alzheimer's disease.
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Markers of Alzheimer's disease (AD) are being widely sought with a number of studies suggesting blood measures of inflammatory proteins as putative biomarkers.
Why it matters
In this study of over 350 subjects, five inflammatory proteins were associated with brain atrophy on MRI, and six analytes changed significantly over one year in people with fast cognitive decline. IL-10 was associated with both clinical and imaging evidence of disease severity and might have potential as a biomarker of progression, but no treatment is tested.
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The findings highlight the regional specificity of the association of WMHs with AD.
Why it matters
In this community study, greater white matter hyperintensity volume in the parietal lobe predicted who went on to develop Alzheimer's disease, while hippocampal volume did not. This suggests that small vessel cerebrovascular disease may play a role in the development of Alzheimer's disease, though it is not clear whether parietal white matter hyperintensities are just a marker of cerebrovascular burden or reflect a distinct type of injury.
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The application of support vector machine classification (SVM) to combined information from magnetic resonance imaging (MRI) and [F18]fluorodeoxyglucose positron emission tomography (FDG-PET) has been shown to improve detection and differentiation of Alzheimer's disease dementia (AD) and frontotemporal lobar degeneration.
Why it matters
This study used a machine learning method with MRI and FDG-PET scans to detect Alzheimer's disease across different clinical centers. It is a diagnostic approach and does not provide a treatment, cure, or prevention.
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Our findings suggest that insulin metabolism influences the clinical manifestation of AD only within 3 years.
Why it matters
In this cohort of people without diabetes at baseline, higher insulin levels and insulin resistance were associated with a higher risk of Alzheimer disease only within the first 3 years, and this increased risk disappeared after 3 years. Fasting glucose was not associated with higher Alzheimer risk, so these findings point to a time-limited link rather than a proven way to prevent or treat the disease.
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A number of new recommendations and good practice points are made, namely in CSF, neuropsychology, neuroimaging and reviewing non-evidence based therapies.
Why it matters
This revised international guideline reviews evidence published before May 2009 and gives graded recommendations for diagnosing and managing Alzheimer's disease. It is a guidance document for clinicians rather than a study of a new treatment or cure.
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We set out to determine factors that influence the rate of brain atrophy in 1-year longitudinal magnetic resonance imaging (MRI) data.
Why it matters
This imaging study found that brain shrinkage rates differ by age and sex, being faster in women and in younger people, and that these rates tracked with amyloid, tau, and ApoE4. It does not test any treatment, but suggests that focusing on women or younger subjects could make clinical trials more efficient.
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.
- A Phase II, Randomized, Double-Blind, Placebo-Controlled Study of Safety, Pharmacokinetics, and Biomarker Results of Subcutaneous Bapineuzumab in Patients with mild to moderate Alzheimer's disease
- A Complementary Dataset of Scalp EEG Recordings Featuring Participants with Alzheimer’s Disease, Frontotemporal Dementia, and Healthy Controls, Obtained from Photostimulation EEG
- Regional Distribution of Mineralized Blood Vessels in Alzheimer Disease and Clinicopathological Associations: A Multicenter Autopsy Study
- Presence of T-cytotoxic suppressor and leucocyte common antigen positive cells in Alzheimer's disease brain tissue
- Single and multiple transgenic mice as models for Alzheimer's disease
- Differing patterns of temporal atrophy in Alzheimer's disease and semantic dementia
- Sex and gender differences in Alzheimer's disease: current challenges and implications for clinical practice: Position paper of the Dementia and Cognitive Disorders Panel of the European Academy of Neurology
- The morphological phenotype of beta-amyloid plaques and associated neuritic changes in Alzheimer's disease
- In vivo and in vitro evidence supporting a role for the inflammatory cytokine interleukin-1 as a driving force in Alzheimer pathogenesis
- Repeated Transcranial Magnetic Stimulation for Improving Cognition in Patients With Alzheimer Disease: Protocol for a Randomized, Double-Blind, Placebo-Controlled Trial