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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Benzodiazepine use is associated with an increased risk of Alzheimer's disease.
Why it matters
In Quebec health-insurance records of adults over 66, the 1,796 people diagnosed with Alzheimer's were more likely than 7,184 matched controls to have started a benzodiazepine at least five years earlier (adjusted odds ratio 1.51; 1.43 after also accounting for anxiety, depression and insomnia), and the link was stronger for long-term use. The authors say this "reinforces the suspicion of a possible direct association" but that benzodiazepine use "might also be an early marker" of a condition that raises dementia risk — so it shows an association, not that the drugs cause Alzheimer's.
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PF-04494700 at 20 mg/d was associated with increased adverse events and cognitive decline.
Why it matters
The high dose of PF-04494700 was associated with confusion, falls, and greater cognitive decline and was discontinued, and the low dose met criteria for futility. The authors conclude that PF-04494700 at 20 mg/d was associated with increased adverse events and cognitive decline.
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To discover susceptibility genes of late-onset Alzheimer's disease (LOAD), we conducted a 3-stage genome-wide association study (GWAS) using three populations: Japanese from the Japanese Genetic Consortium for Alzheimer Disease (JGSCAD), Koreans, and Caucasians from the Alzheimer Disease Genetic Consortium (ADGC).
Why it matters
This genome-wide association study found genome-wide significant association between the SORL1 gene and late-onset Alzheimer's disease across Japanese, Korean, and Caucasian populations. It identifies a genetic risk factor but does not provide a treatment, cure, or prevention.
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The primary efficacy analysis did not show cognitive benefit with huperzine A 200 μg BID.
Why it matters
In this phase II trial, huperzine A at 200 μg twice daily did not affect cognitive change at 16 weeks, and other outcomes were not significant at either dose. This means the study did not show a clear benefit of huperzine A for mild to moderate Alzheimer disease.
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ADNI has demonstrated the feasibility and utility of multicenter PET studies and is helping to clarify the role of biomarkers in the study of aging and dementia.
Why it matters
This 2010 progress report from the ADNI PET Core describes a standardised scanning protocol and image processing that make PET scans from different scanner models comparable; the authors say the protocol "has been widely adopted in academic and pharmaceutical industry studies." In ADNI data, FDG-PET "increases statistical power over traditional cognitive measures" and could reduce clinical-trial sample sizes, and in an add-on of about 100 people, amyloid PET showed expected differences between Alzheimer's, MCI and control groups and identified some people whose amyloid rose significantly each year; no figures are given in the record. It is a research-methods report and does not test any treatment, cure or prevention.
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To test the effects of the PPAR-γ agonist pioglitazone on cognition, regional cerebral blood flow (rCBF), and plasma levels of Aβ40 and Aβ42, we conducted a 6-month, randomized, open-controlled trial in patients with mild Alzheimer disease (AD) accompanied with type II diabetes mellitus.
Why it matters
In this small pilot trial of 42 patients with mild Alzheimer disease and type II diabetes, those given pioglitazone showed cognitive and functional improvements and stabilization of the disease. Because it was a pilot study, these results need confirmation in larger trials.
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Group differences were seen in skin and subcutaneous tissue concerns (P=.05), including 3 possible drug rashes and 3 reports of hair color change in the treatment groups.
Why it matters
This phase 2 safety trial of 51 individuals with mild to moderate Alzheimer disease found that the gamma-secretase inhibitor LY450139 reduced plasma Abeta(40) concentration and was associated with skin and subcutaneous tissue concerns, including possible drug rashes and reports of hair color change. The study was designed primarily to assess safety and tolerability, not to determine whether the treatment improves symptoms.
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Use of naproxen or celecoxib did not improve cognitive function.
Why it matters
In this randomized trial, use of naproxen or celecoxib did not improve cognitive function; naproxen was associated with lower global summary scores over time compared with placebo, and both treatments showed lower scores on the Modified Mini-Mental State Examination. The trial was stopped early, and analyses limited to measures collected while participants were taking study drugs gave similar results.
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69/100
Progression from amnestic mild cognitive impairment to Alzheimer disease in this cohort was best determined by combining four common, easily administered, cognitive measures.
Why it matters
In 539 people with amnestic mild cognitive impairment followed for 36 months in an Alzheimer's Disease Cooperative Study drug trial, 212 progressed to Alzheimer's disease. The best prediction came from combining "four common, easily administered, cognitive measures" (delayed word-list and paragraph recall, the Symbol Digit Modalities Test and the ADAS-cog) with APOE4 status, for an estimated 80% cross-validated accuracy, and dropping APOE4 left accuracy "similar". This is about predicting who progresses, measured within one trial cohort, not about diagnosing an individual or treating, curing or preventing Alzheimer's disease.
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Loneliness is associated with an increased risk of late-life dementia but not with its leading causes.
Why it matters
This cohort study found that loneliness was associated with more than double the risk of developing Alzheimer's disease, and this was not explained by social isolation or brain pathology. It suggests a potential risk factor but does not show that reducing loneliness prevents or treats the disease.
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69/100
The failure of selective cyclo-oxygenase-2 inhibition to slow the progression of AD may indicate either that the disease process is too advanced to modify in patients with established dementia or that cyclo-oxygenase-2 does not play a significant role in the pathogenesis of the disorder.
Why it matters
In this 12-month trial of 692 patients with mild or moderate Alzheimer's disease, the anti-inflammatory drug rofecoxib did not slow dementia progression compared with placebo. There were no significant differences on cognitive or clinician-rated measures, so this drug does not appear to help people who already have Alzheimer's disease.
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An increased plasma homocysteine level is a strong, independent risk factor for the development of dementia and Alzheimer's disease.
Why it matters
In this Framingham Study cohort, elevated plasma homocysteine levels measured at baseline and eight years earlier were associated with an increased risk of newly diagnosed dementia and Alzheimer's disease over a median follow-up of eight years. The study identifies homocysteine as a risk factor but does not test whether lowering it prevents dementia.
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The APOE genotype is an important determinant of the risk of dementia.
Why it matters
In this population-based study, people with the APOE epsilon4/4 genotype had more than a 10-fold higher risk of dementia and those with epsilon3/4 had a 1.7-fold higher risk compared with epsilon3/3. About 20% of dementia cases were estimated to be attributable to the epsilon4 allele, and APOE genotypes explained up to 10% of the variance in age at dementia onset, which informs risk understanding rather than offering a treatment.
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The data suggest that increased educational and occupational attainment may reduce the risk of incident AD, either by decreasing ease of clinical detection of AD or by imparting a reserve that delays the onset of clinical manifestations.
Why it matters
In this 1994 study, 593 people aged 60 or over in North Manhattan, none of whom had dementia, were tested again 1 to 4 years later; 106 developed dementia, all but five of them Alzheimer's disease. After allowing for age and sex, people with low education had about twice the risk (RR 2.02) and people in low-attainment jobs had a similar increase (RR 2.25), with the highest risk in those low on both. The authors say this may mean education and work either make Alzheimer's harder to detect on tests or give a reserve that delays symptoms; it is an association, not proof that more education prevents the disease.
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Known risk factors for Alzheimer's disease (AD) are few and insufficient knowledge is available to recommend steps to reduce AD in our ageing populations.
Why it matters
In this two-year randomized trial of 63 patients with probable Alzheimer's disease, those treated with desferrioxamine showed a slower decline in daily living skills than the untreated group. The authors argue that aluminium may play an active role in the disease process, though they note it is not 'the cause'.
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The BioFINDER-2 main cohort included 872 participants, with an additional 156 participants in the Knight ADRC cohort for independent validation.
Why it matters
A blood-based model using two tau measures matched established PET-based stages of Alzheimer's disease. This is a diagnostic and staging tool, not a treatment, cure or prevention.
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These findings add to growing evidence that women have a differential tau response to Aβ that may emerge at the point of p-tau secretion.
Why it matters
Across five cohorts, women had higher blood p-tau217 levels than men at higher amyloid levels and showed greater tau buildup in several brain regions. The authors say this adds to evidence that women have a different tau response to amyloid, which may emerge early in the disease process.
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In a Chinese cohort of 1,275 people spanning normal cognition to dementia, this study compared three blood markers: p-tau217 rose steadily as amyloid and tau pathology worsened and was very good at both ruling out early disease and flagging advanced tau pathology.
Why it matters
In 1,275 people, blood p-tau217 rose as amyloid and tau pathology worsened and was very good at flagging advanced tau pathology, while GFAP appeared linked to amyloid-driven tau progression and NfL was only weakly tied to Alzheimer's-specific pathology. These are biomarker associations in a cohort, not evidence that measuring or changing them treats or prevents the disease.
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A total of 716 individuals were included in the analysis: 413 cognitively unimpaired (CU) participants (58.6% female; mean age = 70.6 years, SD = 7.9) and 303 cognitively impaired (CI) participants (54.7% female; mean age = 73.2 years, SD = 7.4).
Why it matters
This analysis of 716 people found that changes in plasma p-tau217 over time were similar in cognitively unimpaired and cognitively impaired individuals with amyloid pathology, and it could serve as an endpoint in clinical trials. Selecting people with intermediate amyloid levels reduced the sample sizes needed to detect a drug effect.
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At baseline, 2,279 dementia-free participants with available blood samples were included (median age 72 (interquartile range, 61-81) years; 62% female).
Why it matters
Among 2279 dementia-free older adults, lower eGFR was associated with higher levels of most examined Alzheimer's disease blood biomarkers except Aβ42/40, but impaired kidney function was not associated with an increased hazard of dementia. This means kidney function should be considered when interpreting Alzheimer's blood biomarker results, and it does not show a way to treat, cure, or prevent Alzheimer's disease.
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There were 838 BioFINDER-2 participants (mean age, 73.9 [SD, 7.3] years; 431 women [51%]; 407 men [49%]) and 380 ADNI participants (average age, 72.9 [SD, 7.0] years; 194 women [51%]; 186 mean [49%]) included.
Why it matters
In this evaluation of revised criteria for biological and clinical staging of Alzheimer disease, only 37.7% of the BioFINDER-2 sample had congruent biological and clinical stages, while 51.3% had more advanced clinical impairment than their clinical stage and 11.0% had the opposite. The results highlight the importance of measuring non-AD biomarkers in patients with worse cognitive impairment than expected from their biological stage, which could affect clinical diagnosis and prognosis, but no treatment, cure, or prevention is reported.
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Higher tau levels are associated with the fastest decline in everyday functioning in the presence of elevated amyloid, and those accumulating more tau show a faster decline in everyday functioning.
Why it matters
Among 1,707 cognitively unimpaired older adults, those with elevated amyloid and the highest tau levels showed the largest decline in everyday functioning. The authors suggest that sensitive measures of daily functioning could be useful in clinical practice and trials at the preclinical stage.
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In Alzheimer's disease (AD), amyloid-β (Aβ) triggers the aggregation and spreading of tau pathology, which drives neurodegeneration and cognitive decline.
Why it matters
Combining amyloid PET, resting-state functional MRI and longitudinal tau-PET in controls and amyloid-positive patients, this study found that amyloid-beta induces hyperconnectivity of temporal lobe tau epicenters to vulnerable posterior brain regions, and that this precedes neocortical tau spreading. It identifies a mechanism by which amyloid-beta promotes tau spread, which may inform therapeutic efforts, but no treatment is tested.
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This large multi-country study tested a fully automated, commercially available blood test (Lumipulse platform, measuring p-tau217) in nearly 1,800 people across memory clinics and, notably, primary care doctors' offices in Sweden, Spain, and Italy.
Why it matters
A fully automated blood test classified Alzheimer's amyloid pathology correctly in roughly 85-94% of people, including in primary care settings, and a two-cutoff approach could cut confirmatory spinal fluid testing by up to 60%. This is a cross-sectional diagnostic study, so it shows the test can help identify disease but does not treat or prevent it.
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Of 47 participants enrolled (mean age = 73.8 years; 43% female), 1 dropped out before treatment initiation and 6 before completion, including 2 in the nicotinamide and 4 in the placebo arm.
Why it matters
In this small 47-person trial, nicotinamide showed no significant benefit on the main biomarker outcome, and no significant effects on other biomarkers or on cognitive and functional measures. One measure of decline favored nicotinamide but was not adjusted for multiple comparisons, so the trial does not show that nicotinamide treats early Alzheimer's disease.
From across this topic
9 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 9. The same 9 appear here every time.
- The implications of different approaches to define AT(N) in Alzheimer disease
- Comparison of plasma p‐tau217 and Aβ42/Aβ40 biomarkers by race to detect Alzheimer’s disease
- Revisiting DLB Diagnosis: A Consideration of Prodromal DLB and of the Diagnostic Overlap With Alzheimer Disease
- Quantification of amyloid PET for future clinical use: a state-of-the-art review
- Retinal fluorescence lifetime imaging ophthalmoscopy measures depend on the severity of Alzheimer's disease
- Morphologic and biochemical analysis of the intracellular trafficking of the Alzheimer beta/A4 amyloid precursor protein
- Clinical meaningfulness of anti-amyloid therapies in early Alzheimer's disease: Perspectives from the East and Southeast Asia region
- Stacked CNN-based multichannel attention networks for Alzheimer disease detection
- [Biochemical markers for Alzheimer disease]