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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Late Onset Alzheimer's disease (LOAD) is the leading cause of dementia.
Why it matters
This study used genome-wide association data to point to the immune system and cholesterol metabolism as processes involved in late-onset Alzheimer's disease. It identifies biological pathways rather than testing any treatment, cure, or prevention.
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We present evidence of AD-induced changes in global brain functional connectivity specifically affecting long-distance connectivity.
Why it matters
In 18 mild Alzheimer patients compared with 21 healthy controls, the characteristic path length of functional brain networks was closer to random networks, while no significant differences were found in cluster coefficient. This suggests a loss of global information integration in the disease.
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Genome-wide association studies (GWAS) of late-onset Alzheimer disease (LOAD) have consistently observed strong evidence of association with polymorphisms in APOE.
Why it matters
This case-control genetic study confirmed the APOE risk effect and found a significant association between late-onset Alzheimer's disease and a variant in the MTHFD1L gene on chromosome 6, which is involved in folate metabolism. This identifies a possible genetic risk factor and a link to folate pathways, but it does not show that changing folate intake prevents or treats Alzheimer's disease.
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This risk score could be used to identify persons at risk of LOAD, but can also be used to adjust for confounders in epidemiologic studies.
Why it matters
This study developed a vascular risk score including age, sex, education, ethnicity, APOE epsilon4, diabetes, hypertension or smoking, HDL levels, and waist-to-hip ratio that predicted late-onset Alzheimer's disease in a New York cohort. It is a risk prediction tool and the authors note it needs validation in other populations; it is not a treatment or prevention.
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An (18)F-labeled PET amyloid-beta (Abeta) imaging agent could facilitate the clinical evaluation of late-life cognitive impairment by providing an objective measure for Alzheimer disease (AD) pathology.
Why it matters
This small open-label study gave the amyloid PET tracer florbetapir (18F-AV-45) to 16 people with Alzheimer's disease and 16 cognitively healthy controls, scanning for about 90 minutes and calculating uptake ratios against the cerebellum. The authors' rationale was that such a tracer "could facilitate the clinical evaluation of late-life cognitive impairment," but the text held here stops at the methods, so it reports no imaging, accuracy or safety results. It is a scan study, not a test of any treatment.
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56/100
The Australian Imaging, Biomarkers and Lifestyle (AIBL) study performed (11)C-Pittsburgh Compound B (PiB) scans in 177 healthy controls (HC), 57 mild cognitive impairment (MCI) subjects, and 53 mild Alzheimer's disease (AD) patients.
Why it matters
Amyloid imaging results from the Australian Imaging, Biomarkers and Lifestyle study of aging. Imaging describes what is present in participants' brains; no treatment is given or tested.
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Structural imaging based on magnetic resonance is an integral part of the clinical assessment of patients with suspected Alzheimer dementia.
Why it matters
Structural MRI can help diagnose Alzheimer's and other dementias and is used to track brain shrinkage in trials of potential disease-modifying therapies. It is a diagnostic and monitoring tool, not itself a treatment or cure.
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56/100
Patients with dementia were older and had higher rates of hypertension, coronary artery disease, renal failure, heart failure, and prior strokes.
Why it matters
Among 37,025 patients in a heart-care database followed for about five years, those with atrial fibrillation were more likely to develop every dementia type the study tracked, including Alzheimer's. The authors report the Alzheimer's link was strongest in younger patients, and that AF also marked people with dementia who were at higher risk of death. This is an observational association: it does not show that AF causes dementia, or that treating AF would prevent it.
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Treatment success in Alzheimer disease (AD) trials is generally based on benefits over placebo-treated controls.
Why it matters
Pooled data from 13 donepezil trials found that placebo-treated patients declined more slowly in more recent trials than in older trials, while donepezil's treatment effects stayed consistent. This is about how trial results may vary over time, not about curing or preventing Alzheimer's disease.
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PIB-positive subjects with mild cognitive impairment (MCI) are significantly more likely to convert to AD than PIB-negative patients, faster converters having higher PIB retention levels at baseline than slower converters.
Why it matters
In 31 people with mild cognitive impairment followed for 1 to 3 years, 14 of the 17 whose PIB PET brain scan showed raised amyloid were diagnosed with Alzheimer's disease, compared with 1 of the 14 whose scan did not. The authors conclude the scan "provides useful prognostic information"; among the amyloid-positive group, faster converters had higher amyloid in frontal regions, and an APOE ε4 link to faster conversion was seen in the 17 people with known genotype. This is a small prediction study that shows an association; it does not test a treatment or show that amyloid causes the decline.
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Why it matters
Describes the neuropathology of aging without dementia, presented as presumptive evidence for preclinical Alzheimer disease.
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Physical frailty in old age is associated with Alzheimer disease pathology in older persons with and without dementia.
Why it matters
In 165 autopsied participants, Alzheimer disease pathology was associated with physical frailty near death, though it accounted for only 4% of the variance, while cerebral infarcts and Lewy bodies were not. This links Alzheimer pathology to frailty but does not show that treating the pathology would improve frailty.
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Alzheimer's disease is the most common dementia and is pathologically characterized by deposition of amyloid-beta peptide (Abeta) into beta-amyloid plaques, neuronal injury and low-level, chronic activation of brain immunity.
Why it matters
In a mouse model of Alzheimer's disease, blocking TGF-beta-Smad2/3 innate immune signaling reduced Alzheimer-like pathology. This is an animal study, so it does not show that the same approach would treat, cure, or prevent Alzheimer's disease in people.
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Persons with dementia suffer different losses at different stages of the disease and therefore accurate assessment of abilities and losses is critical to assist the person in planning for their future and for care needs.
Why it matters
This is a design and baseline report of a two-year trial testing a specific care and assistance plan against usual care in 1120 people with Alzheimer's disease in France. No results on whether the plan changes functional capacity are reported here, so it does not yet show any effect on treating, curing or preventing the disease.
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56/100
Alzheimer's disease and frontotemporal dementia (FTD) can be difficult to differentiate clinically because of overlapping symptoms.
Why it matters
This imaging study found different patterns of cortical thinning in Alzheimer's disease and frontotemporal dementia and that cortical thickness related to cognitive impairment. It is about improving diagnosis, not about treating, curing or preventing Alzheimer's disease.
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Ninety-nine new cases of dementia (including 71 of Alzheimer disease) occurred during the follow-up.
Why it matters
Among 899 dementia-free adults in the Framingham Heart Study (median age 76, followed for an average of 9.1 years), those whose blood DHA, a fatty acid found mostly in fatty fish, was in the top quarter had about half the risk of developing any dementia compared with everyone else (relative risk 0.53, 95% CI 0.29–0.97), after accounting for age, sex, APOE ε4, homocysteine and education. The result for Alzheimer disease alone was smaller and not statistically clear (0.61, 95% CI 0.31–1.18). This was an observational study that measured blood levels once; it shows an association, not that taking DHA or eating more fish prevents dementia.
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56/100
The results suggest that difficulty in identifying familiar odours in old age is partly due to the accumulation of neurofibrillar pathology in central olfactory regions.
Why it matters
In this autopsy study, difficulty identifying familiar odors in old age was partly related to the buildup of tau tangles and other Alzheimer's disease pathology in the brain. This links a simple smell test to brain pathology but does not test any treatment, cure or prevention.
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We conclude that higher adherence to the MeDi is associated with a reduction in risk for AD.
Why it matters
Among 2,258 people in New York without dementia, followed for an average of 4 years, higher adherence to the Mediterranean diet was associated with a lower risk for Alzheimer's disease. People in the highest tertile of adherence had a lower risk than those in the lowest.
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The APOE epsilon4 allele appears to be associated with a higher prevalence of dementia in PD.
Why it matters
This meta-analysis of case-control studies found that the APOE4 allele appears to be associated with a higher prevalence of dementia in Parkinson disease. The authors note publication bias and heterogeneity in the source data, so the finding should be interpreted with caution.
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According to all previous literature, they are not associated with mortality.
Why it matters
In 456 patients with early Alzheimer disease followed for up to 14 years, delusions and hallucinations were examined for their ability to predict outcomes such as cognitive decline, functional decline and institutionalization. This is about predicting how the disease progresses, not about treating, curing or preventing it.
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We prospectively evaluated the diagnostic accuracy of cerebrospinal fluid (CSF)-beta-amyloid1-42 (Abeta42), -total-tau (tau) and -phosphorylated-tau181 (p-tau181) as measured by sandwich ELISAs in the clinical routine of a community state hospital to discriminate between patients with Alzheimer's disease (AD), healthy controls (HC), non-AD-dementias, a group composed of various psychiatric disorders (non-AD-dementias, mental diseases) and an age-matched random sample (RS) (total N=219).
Why it matters
This study tested how well cerebrospinal fluid tau, p-tau181, and Aβ42 measurements distinguished Alzheimer's disease patients from healthy controls and other groups in a hospital setting. It is about diagnostic accuracy of these fluid markers, not about treating, curing, or preventing Alzheimer's disease.
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Alzheimer disease was responsible for 4.9% of the deaths in this elderly cohort.
Why it matters
Following 1,670 adults aged 65 and older in a largely blue-collar rural community in southwestern Pennsylvania for 15 years, this study found that people with Alzheimer disease had a higher risk of death after adjusting for other factors (hazard ratio 1.4), and it estimated that AD accounted for 4.9% of deaths in the cohort. When men and women were analysed separately, the increased risk showed up only in women. Death certificates of people with AD more often listed dementia, other brain disorders, pneumonia and dehydration, and less often cancer. The study is observational and from one community, so it describes an association there; it does not test any treatment or prevention.
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56/100
Family history of dementia was associated with an increased risk of dementia and AD in this very old population, but only among APOE epsilon4 carriers.
Why it matters
In 907 non-demented people aged 75 or older followed for six years, having at least two siblings with dementia was linked to a higher risk of Alzheimer's disease. Among APOE4 carriers, those with two or more affected first-degree relatives had increased risk, while no increased risk was seen in non-carriers, suggesting family history and APOE4 together raise risk.
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56/100
Fluorodeoxyglucose positron emission tomography (PET) studies have found that patients with Alzheimer's dementia (AD) have abnormally low rates of cerebral glucose metabolism in posterior cingulate, parietal, temporal, and prefrontal cortex.
Why it matters
APOE ε4 is "a common susceptibility gene for late-onset Alzheimer's dementia", and the authors had earlier found that healthy late-middle-aged carriers show low brain glucose use in the same regions as people with Alzheimer's. This study asked whether that pattern is already present at ages 20–39, comparing 12 carriers (all with one ε4 copy) with 15 non-carriers using memory and thinking tests, MRI and PET. The record we hold describes the question and methods but not the results; it tested no treatment and cannot show that carriers will develop Alzheimer's.
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MRI volumes measured over time are valid biomarkers of pathologic progression of AD across a range of antemortem clinical states.
Why it matters
In 39 subjects followed to death, rates of total brain volume loss and ventricular enlargement were related to postmortem Alzheimer pathology such as tangles and plaques. The authors propose these MRI measures could monitor disease progression or response to treatment, but the study itself tested no treatment.
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.
- Meta-analysis confirms CR1, CLU, and PICALM as alzheimer disease risk loci and reveals interactions with APOE genotypes
- Association of Rare APOE Missense Variants V236E and R251G With Risk of Alzheimer Disease
- The dynamics of cortical and hippocampal atrophy in Alzheimer disease
- Ceperognastat in Early Symptomatic Alzheimer Disease: A Randomized Clinical Trial
- Reduced lean mass in early Alzheimer disease and its association with brain atrophy
- Early-Stage Alzheimer's Disease Prediction Using Machine Learning Models
- Physical activity reduces hippocampal atrophy in elders at genetic risk for Alzheimer's disease
- Mild to moderate Alzheimer dementia with insufficient neuropathological changes
- Can dietary patterns prevent cognitive impairment and reduce Alzheimer's disease risk: Exploring the underlying mechanisms of effects
- Memantine treatment in patients with moderate to severe Alzheimer disease already receiving donepezil: a randomized controlled trial