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.
-
Plasma p-tau217/Aβ42 had high accuracy to detect AD, with comparable performance across race.
Why it matters
Plasma p-tau217/Aβ42 had high accuracy for detecting amyloid PET positivity and performed comparably in Black and White participants, with no significant difference in classification by race. False negatives were more likely to be cognitively normal, which is a limitation to consider when using this test.
-
64/100
The trajectories of core Alzheimer disease (AD) cerebrospinal fluid (CSF) biomarkers and the concurrent cognitive changes across the clinical spectrum remain unclear yet are important for clinical trial design.
Why it matters
This long-term cohort study mapped how spinal fluid amyloid, tau, and cognitive measures change over time across the clinical spectrum of Alzheimer's disease. It is an observational study designed to inform clinical trial design, not to test a treatment or cure.
-
APOE shows a heterogeneous effect on ADRD risk in our Hispanics/Latinos sample, the largest to date.
Why it matters
Among 12,221 Hispanics/Latinos, the APOE ε4 effect on Alzheimer's disease and related dementias risk varied across groups, strongest in Peruvians/Bolivians and weakest in Caribbean-Hispanics. The ε4 effect was replicated in an independent Peruvian cohort, and ε4 carriers had higher dementia conversions and p-tau levels.
-
In the prospective GLORIA-AF registry of AF patients, the presence of clinical complexity was associated with lower odds of being prescribed with OAC (odds ratio [OR] 0.50, 95% confidence interval [CI] 0.44–0.57), higher OAC discontinuation, and with a higher risk of adverse events (hazard ratio [HR] 1.63, 95% CI 1.43–1.86).[ 4 ] Indeed, “high clinical complexity” patients defined using latent class analysis constituted 6.6% of AF patients, and was associated with higher hazards of experiencing the primary composite outcome of all-cause death and major adverse cardiovascular events (HR 1.47, 95% 1.24–1.75).[ 5 ] Comorbidities and polypharmacy have an important influence on decision-making, by conditioning either lack of prescription of OAC in patients at risk or inappropriate dosing.[ 6 ] [ 7 ] [ 8 ] Recognizing that AF management is more than simply OAC alone, and requires a holistic and integrated care approach, contemporary guidelines globally on AF management have promoted this concept, based on the Atrial fibrillation Better Care (ABC) pathway, emphasizing Anticoagulation, Better symptom management with rate or rhythm control, and Comorbidity/lifestyle management.[ 9 ] [ 10 ] [ 11 ] The ABC pathway is well supported by clinical trial and real-world evidence,[ 11 ] whereby adherence to the ABC pathway is associated with a reduction in all-cause and cardiovascular mortality, stroke, and bleeding.[ 12 ] [ 13 ] Despite this, adherence to ABC-based management remains low, whereby a meta-analysis of 14 studies revealed that only 21% (95% CI 13–34%) of AF patients were managed in accordance with the ABC pathway.[ 12 ] This perhaps highlights a critical gap in the implementation of comprehensive evidence-based care strategies.
Why it matters
This describes a European consortium plan to use AI to manage the complexity and comorbidities of patients with atrial fibrillation, a condition linked to higher risk of dementia among other outcomes. It reports no treatment, cure, or prevention of Alzheimer's disease.
-
64/100
Our findings revealed distinct patterns of connectivity linked to normal ageing or Alzheimer's disease.
Why it matters
This longitudinal study found that Alzheimer's disease was characterised by hyperconnectivity in the anterior-temporal network, which was associated with amyloid burden, glucose hypometabolism, hippocampal atrophy and cognitive deficits. It describes a pattern of brain connectivity and does not test any treatment, cure or prevention.
-
Higher levels of P-tau181 (HR = 1.32 [95% CI: 1.17-1.51]), NfL (HR = 1.19 [95% CI: 1.03-1.36]), and GFAP (HR = 1.36 [95% CI: 1.22-1.52]), and a lower Aβ42/Aβ40 ratio (HR = 0.80 [95% CI: 0.68-0.95]) were associated with an increased risk of progressing to clinically-diagnosed DAT.
Why it matters
In 1,007 people aged 79-94 without dementia from primary care, higher P-tau181, NfL, and GFAP and a lower Aβ42/Aβ40 ratio were linked to greater risk of later Alzheimer's dementia and faster cognitive decline. Combining a brief cognitive test with these blood markers improved identification of who would develop dementia.
-
Nonlinear dose-response relationship between exercise and cognitive improvement in Alzheimer's disease, with the optimal AE dose identified at 660 METs-min/week for enhancing cognitive function in AD.
Why it matters
This meta-analysis of 27 studies with 2,242 Alzheimer's disease patients found a nonlinear relationship between exercise and cognitive improvement, with the best results at a dose of 650 METs-min/week and aerobic exercise appearing particularly effective. It suggests that specific exercise doses may help cognitive function in people who already have Alzheimer's disease, but it does not show that exercise prevents or cures the disease.
-
Alzheimer's disease (AD) is heterogenous at the molecular level.
Why it matters
Using mass spectrometry proteomics of cerebrospinal fluid from 419 people with Alzheimer's disease and 187 controls, this study defined five molecular subtypes with distinct genetic risk profiles and different affected processes, such as innate immune activation. It identifies disease heterogeneity relevant to drug development but does not itself report a treatment, cure or prevention.
-
Sleep duration is linked to amyloid-β clearance while physical activity is associated with brain volume maintenance.
Why it matters
In 4322 participants, sleep duration was associated with cognition through amyloid burden and physical activity through brain volume, with these paths being independent. This is about how lifestyle factors relate to cognition via brain pathology and structure, not a proven way to prevent or cure Alzheimer's disease.
-
Low hemoglobin and anemia are associated with cognitive impairment and Alzheimer's disease (AD).
Why it matters
This large UK Biobank study examined links between blood cell indices, anemia, and the risk of developing dementia, using Mendelian randomization to look for causal associations. It identifies possible risk markers but does not test any treatment or prevention for dementia.
-
Our study indicates that changes in PVS-related MRI parameters occur in MCI and AD, possibly due to impairment of the glymphatic system.
Why it matters
In this small comparison of 36 patients with Alzheimer disease, 44 with mild cognitive impairment, and 31 healthy controls, MRI measures related to the brain's perivascular network differed between groups and correlated with amyloid deposition and worse cognitive performance. These findings are preliminary and do not show that targeting this system would treat or prevent Alzheimer disease.
-
Among cognitively normal participants with positive biomarkers, 34.4% developed cognitive impairment (Clinical Dementia Rating > 0) as compared to 8.4% of those with negative biomarkers.
Why it matters
Among cognitively normal people, those with positive preclinical Alzheimer's biomarkers were more likely to develop cognitive impairment than those with negative biomarkers, and biomarker status, APOE ɛ4 carrier status, polygenic risk score and age influenced that risk. This supports the idea that biomarkers can predict who will develop cognitive problems, but it does not show that any treatment, cure or prevention works.
-
Blood biomarkers indicative of Alzheimer's disease (AD) pathology are altered in both preclinical and symptomatic stages of the disease.
Why it matters
In the BioFINDER-1 cohort, blood p-tau231 and the amyloid-beta 42/40 ratio were more changed at lower levels of amyloid pathology, but only p-tau217 rose markedly over 4-6 years and its increases were associated with cognitive decline and brain atrophy. This was confirmed in a second cohort, and the authors highlight p-tau217 as a marker of disease progression in preclinical and prodromal Alzheimer's disease.
-
This study aimed to examine whether baseline CSF measures of Alzheimer disease (AD)-related pathology are associated with the time to onset of mild cognitive impairment (MCI) and whether these associations differ by age, sex, Apolipoprotein E ( ApoE4 ) status, and proximal (≤7 years) vs distal (>7 years) time to symptom onset.
Why it matters
In the BIOCARD longitudinal study, baseline cerebrospinal fluid measures of amyloid and tau were examined for their relationship with time to onset of mild cognitive impairment, including differences by age, sex and ApoE4 status. The findings are about predicting symptom onset, not about any treatment or cure.
-
These results confirm the absence of a neurocognitive risk associated with statin treatment and suggest a potential favourable role of statins.
Why it matters
This meta-analysis of observational studies found that statin use was associated with a decreased risk of dementia and of Alzheimer's disease. Because it pools observational studies, it cannot show that statins prevent or treat Alzheimer's disease.
-
Improved insight into these pathomechanisms may allow to shed light on the role of Aβ deposition as a primary versus a secondary event in the complex pathogenesis of AD.
Why it matters
This review of human studies examines evidence of blood-brain barrier dysfunction in Alzheimer's disease and how it may relate to amyloid deposition. It is a summary of research that may inform understanding of the disease process, not a treatment or cure.
-
The 4417 participants in the study included 2618 women (59%) and had a mean (SD) age of 71.3 (4.7) years.
Why it matters
In 4,417 older adults (mean age 71), people who reported sleeping less had more amyloid-β on PET scans, and those sleeping 6 hours or less scored lower, mostly on memory tests. Both short (≤6 h) and long (≥9 h) sleepers had higher body mass index than 7–8 hour sleepers, and short sleepers reported more depressive symptoms. Because sleep was self-reported and everything was measured at a single time point, the study cannot say whether poor sleep drives amyloid or the reverse, and it does not show that changing sleep prevents Alzheimer's.
-
In 303 participants (mean [SD] age, 73.16 [5.19] years, 181 [60%] women, 96 [32%] non-Hispanic White, 113 [37%] Non-Hispanic Black, 94 [31%] Hispanic), baseline WMH volumes were associated with cortical thinning in medial temporal and frontal/parietal regions.
Why it matters
In 303 older adults from northern Manhattan who had two MRI scans about 4 years apart, people with more white matter hyperintensities (an MRI sign of small blood vessel disease) at the start went on to show more thinning of the cortex in areas typical of Alzheimer's disease, including the entorhinal cortex in the medial temporal lobe. The authors report this link was seen "particularly among non-Hispanic Black older adults" and suggest blood vessel disease "may" add to Alzheimer's progression by promoting brain cell loss. This is an observational association, not proof of cause, and the study did not test any treatment or prevention.
-
Previous studies have suggested that the APOE ɛ4 allele plays a role in the risk and age at onset of dementia in DS; however, data on in vivo biomarkers remain scarce.
Why it matters
In adults with Down syndrome, carrying the APOE ɛ4 allele was associated with earlier clinical and biomarker changes of Alzheimer's disease. It is an observational cohort study and does not test any treatment, cure or prevention.
-
Importantly, they suggest that these associations might be explained by a decrease of amyloidosis and tau-pathology.
Why it matters
In this cross-sectional study, higher adherence to a Mediterranean-like diet was linked to larger mediotemporal gray matter volume and better memory, and these links appeared to be explained by lower amyloid and tau pathology. Because the study looked at people at one point in time, it cannot prove that the diet prevents Alzheimer's disease, and the authors call for longitudinal and dietary intervention studies.
-
64/100
Why it matters
Gives the International Working Group's recommendations for the clinical diagnosis of Alzheimer's disease.
-
Online education involving a celebrity may be an effective strategy for educating college students about AD risk reduction strategies.
Why it matters
This randomized trial tested online Alzheimer's education for high school and college students and found that celebrity-led formats improved quiz scores among college students. The study is about education and awareness in young people, not about treating, curing, or preventing Alzheimer's disease.
-
The sample consisted of 447 decedents (249 men [56%]; mean [SD] age, 80.3 [9.5] years; median year of death, 2011) spanning 24 years of donation.
Why it matters
In 447 brain donors (mean age at death 80), each one-decile step up the Area Deprivation Index was associated with about 8% higher odds of Alzheimer disease neuropathology at autopsy (adjusted odds ratio 1.08), which the authors translate into roughly 2.2 times the odds for the most disadvantaged decile (adjusted odds ratio 2.18). This is a cross-sectional association, not evidence that neighbourhood causes the disease, and only 24 donors (5.4%) came from the most disadvantaged fifth of neighbourhoods. The authors describe it as the first link between neighbourhood disadvantage and Alzheimer neuropathology and as a method that "has the potential to be applied to any brain bank within the United States."
-
Alzheimer's disease (AD) is an incurable neurodegenerative disorder accounting for 70%-80% dementia cases worldwide.
Why it matters
This study developed a deep learning approach using resting-state fMRI to classify Alzheimer's disease stages. It is a diagnostic tool development study and does not test any treatment, cure, or prevention.
-
The amyloid/tau/neurodegeneration (A/T/N) framework uses cerebrospinal fluid (CSF) levels of total tau (tTau) as a marker of neurodegeneration and CSF levels of phosphorylated tau 181 (pTau181) as a marker of tau tangles.
Why it matters
This cohort study examined how cerebrospinal fluid total tau and phosphorylated tau 181 change over the course of Alzheimer's disease and how those changes relate to brain atrophy. It is observational and does not test any treatment or prevention.
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.
- Bone density and brain atrophy in early Alzheimer's disease
- Factors affecting Aβ plasma levels and their utility as biomarkers in ADNI
- Alzheimer's disease and dementia in Japan: Epidemiological trends, regional disparities, and future projections
- Frequency of Stages of Alzheimer-Related Lesions in Different Age Categories
- 18F-FDG PET Improves Diagnosis in Patients with Focal-Onset Dementias
- Artificial Intelligence Assistive Software Tool for Automated Detection and Quantification of Amyloid-Related Imaging Abnormalities
- Lewy- and Alzheimer-type pathologies in Parkinson's disease dementia: which is more important?
- Generation of Alzheimer beta-amyloid protein in the trans-Golgi network in the apparent absence of vesicle formation
- Tau PET patterns mirror clinical and neuroanatomical variability in Alzheimer's disease
- Crystal structure of the N-terminal, growth factor-like domain of Alzheimer amyloid precursor protein