Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Highest usefulness score first. Studies without a score come last.
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Alzheimer's disease has been thought to have familial and sporadic forms, and several genetic defects have been identified that chiefly explain early-onset familial cases.
Why it matters
This Swedish twin registry study was designed to find all cases of dementia in the registry and estimate how much of the liability to Alzheimer's disease is due to genetic factors. It estimates genetic contribution only and does not provide a treatment, cure, or prevention for Alzheimer's disease.
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Apolipoprotein E (apoE) is critical in the modulation of cholesterol and phospholipid transport between cells of different types.
Why it matters
This study found that the number of APOE epsilon 4 alleles was linked to lower cholinergic markers in the brains of people with Alzheimer's disease. In a small tacrine trial, most APOE epsilon 4-negative patients improved while most carriers worsened, suggesting the allele may predict poor response to this type of therapy.
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Cultured brain cells are capable of generating many molecules associated with inflammatory and immune functions.
Why it matters
This 1995 review describes what it calls "the endogenous immune response system of brain": molecules such as complement proteins, inflammatory cytokines, acute phase reactants and proteases that cultured brain cells can make, mostly microglia and astrocytes "but even neurons". It reports that many of these appear alongside Alzheimer disease lesions, which it reads as a sign of "chronic inflammation in Alzheimer disease brain". That is an association, not proof of cause. The title points to "implications for therapy", but no treatment is described in the text held here, so nothing in this record shows any drug works.
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Cholinergic markers, neuropeptides, and amines and their metabolites were sampled from identical specimens across 10 neocortical regions in a large sample of Alzheimer's disease (AD) cases and controls.
Why it matters
This study found that cholinergic deficits, particularly choline acetyltransferase activity, were highly correlated with clinical dementia ratings across the neocortex in Alzheimer's disease cases. It suggests that of all the neurochemical species quantified, the cholinergic indices may be the most closely related to dementia severity.
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The purpose of this study was to investigate the prevalence of dementia in an Italian population using a door-to-door 2-phase design.
Why it matters
In a door-to-door survey of all 778 people over age 59 in the Italian town of Appignano in 1987, about 6 in every 100 had dementia (48 people). Alzheimer's disease (2.6 per 100) was only slightly more common than multi-infarct dementia (2.2 per 100), and which type led varied by age group. Rates rose steeply with age; the authors' comparison with other studies suggested dementia was as frequent here as elsewhere and that Alzheimer's "might" be more frequent in rural areas, which this single-town study could not test directly.
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Clinically diagnosed Alzheimer's disease and other dementing illnesses were assessed in a geographically defined US community.
Why it matters
In a US community, 3623 people over 65 had brief memory testing at home and a sample of 467 had full clinical exams. An estimated 10.3% of those over 65 had probable Alzheimer's disease, rising from 3.0% at ages 65 to 74 to 47.2% of those over 85.
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Speech and language assessment in 30 patients with dementia of the Alzheimer type and in 70 normal controls revealed that all Alzheimer patients were aphasic.
Why it matters
In this small study of 30 patients, all those with dementia of the Alzheimer type showed language problems (aphasia), and the problems worsened as dementia became more severe. The authors conclude that aphasia is an important diagnostic criterion for this type of dementia.
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Among the more than 90 identified genetic risk loci for late-onset Alzheimer's disease (AD) and related dementias, the apolipoprotein E (APOE) gene ɛ2/ɛ3/ɛ4 polymorphisms remain the longstanding benchmark for genetic disease risk with a consistently large effect across studies 1-10 .
Why it matters
By analyzing genes separately in APOE ε4 and ε2 carriers, the study found new genetic signals for Alzheimer's risk, including DDHD1. This is genetic risk research that may inform future targeted therapies, not a treatment or cure.
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Cerebral amyloid angiopathy (CAA) is currently diagnosed using MRI-based Boston criteria.
Why it matters
This retrospective multicenter cohort study investigated whether cerebrospinal fluid β-amyloid 1-42 and β-amyloid 1-40 relate to hemorrhagic and nonhemorrhagic MRI markers of disease severity in probable cerebral amyloid angiopathy. It concerns measuring disease severity in a related condition, not treating, curing, or preventing Alzheimer's disease.
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Primary age-related tauopathy (PART) is a β-amyloid-independent tauopathy, thought by some to be a distinct process from Alzheimer disease neuropathologic change (ADNC).
Why it matters
In people with definite or possible primary age-related tauopathy, Alzheimer's-related pathologies did not significantly contribute to cognitive impairment; decline was instead linked to other comorbid pathologies such as TDP-43, Lewy bodies and arteriolosclerosis. This suggests that primary age-related tauopathy alone does not significantly impair cognition, but much of the variance in decline remained unexplained.
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Alzheimer disease (AD) risk differs across ancestral populations, yet most genetic studies have focused on non-Hispanic White (NHW) cohorts.
Why it matters
This study combined genetic and gene activity data across White, African American, and Hispanic participants and prioritized nine genes, including known Alzheimer's loci BIN1, PTK2B, and DMPK. It shows that including multiple populations can improve the precision of genetic studies and help resolve shared and population-specific regulatory mechanisms.
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Lecanemab reduced clinical decline by roughly 27% over placebo, with ARIA-E in 12.6% of treated patients;donanemab slowed decline by about 35%, with ARIA-E near 24%.
Why it matters
Lecanemab and donanemab give modest but genuine slowing of decline in early Alzheimer disease, while aducanumab trials gave discordant results. Safe use depends on genotype-informed eligibility screening and structured serial MRI monitoring because of ARIA risk, which rises several-fold in APOE4 homozygotes.
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HRU and payments were overall similar between A4 and LEARN Medicare.
Why it matters
In this cohort study, individuals with cognitively unimpaired Alzheimer's disease in the A4 Medicare group did not have increased healthcare utilization and payments compared with the LEARN group overall, but those with claims indicators of Alzheimer's disease progression had significantly greater utilization and payments. The authors state that additional research is needed on the health and economic impacts of progression and the potential cost savings associated with effective therapy that delays progression.
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Three trajectory classes were identified: stable, slow decliners, and fast decliners.
Why it matters
This longitudinal study identified three cognitive trajectory classes in preclinical Alzheimer's disease: stable, slow decliners, and fast decliners, with about 70% of amyloid-positive individuals remaining stable. Higher p-tau217, smaller hippocampal volume, and elevated tau PET were associated with the declining classes, which the authors say has important implications for prevention trial design.
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50/100
This cohort study examines the association of serum hyperphosphorylated tau and neurofilament light chain concentrations with psychosis in Alzheimer disease.
Why it matters
This cohort study examined whether serum hyperphosphorylated tau and neurofilament light chain concentrations are associated with psychosis in Alzheimer's disease. It is an observational look at a possible link, not a treatment, cure or prevention.
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Four thousand four hundred eighty-six participants were included (mean age 71.3 ± 4.7 years, 30% participants Aβ+, 59% female).
Why it matters
In this cross-sectional analysis of 4,486 A4 study participants, frailty prevalence in preclinical Alzheimer's disease was 22%, and amyloid-positive participants were more likely to be frail than amyloid-negative ones. Frail participants had lower cognitive scores, but frailty did not influence the relationship between amyloid status and cognition, and the authors say further study is needed.
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Plasma biomarkers may aid Alzheimer disease (AD) diagnosis and prognosis.
Why it matters
This study explored whether cardiovascular risk changes the link between plasma Alzheimer's biomarkers and cognitive status in a large multisite cohort. It is about how biomarkers are interpreted, not about treating, curing or preventing the disease.
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= 0.038) over time. Physical activity was associated with less synaptic dysfunction and cognitive activity with less synaptic dysfunction and lower amyloid burden over time, albeit effect sizes were small.
Why it matters
In this longitudinal study, physical activity was associated with less synaptic dysfunction and cognitive activity with less synaptic dysfunction and lower amyloid burden over time, though effect sizes were small. The authors state that further research is needed to validate the findings and clarify causal inference.
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50/100
Our study included 74,275 weeks of driving data (2015-2024, average follow-up 6.1 years).
Why it matters
This longitudinal study found that greater white matter hyperintensity burden was linked to reduced driving complexity over time, and that this effect was strongest for lesions in the parietal and occipital regions. The authors suggest white matter hyperintensities could serve as a biomarker for identifying people at higher risk of unsafe driving, though the findings concern driving behavior rather than treating or curing Alzheimer's disease itself.
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Clinical stages showed a progressively increased prevalence of Aβ-positivity and higher entorhinal tau PET pathology from cognitively normal (CN) to SOCD, MCI, and dementia in both tracers.
Why it matters
This study compared two tau PET tracers for staging Alzheimer's disease and found moderate agreement between biological and clinical staging with either tracer. It is a diagnostic comparison study and does not test any treatment, cure, or prevention.
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Functional impairment increased progressively from normal cognition to dementia.
Why it matters
This cross-sectional study found that functional impairment increased progressively from normal cognition to dementia, with Alzheimer's disease more associated with memory-dependent tasks and frontotemporal dementia showing disproportionate deficits in executive and social activities. It is about functional profiles, not about treating, curing or preventing dementia.
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= 0.006). Univariable MR analyses indicated that education and participation reduced the risk of AD.
Why it matters
This Mendelian randomization analysis suggested education and participation reduced Alzheimer disease risk, while education also appeared to increase risk of AD/ADRD, which the authors attribute to inconsistencies between clinical and proxy diagnoses. The authors suggest the protective effect of education may be due to other biological mechanisms such as cognitive reserve, and no treatment was tested.
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We assessed 452,718 patients (mean age: 67.16 years).
Why it matters
This retrospective cohort study found that traumatic brain injury was significantly associated with an increased risk of Alzheimer's disease dementia progression and a higher risk of behavioral and psychological symptoms of dementia following diagnosis. It underscores the importance of traumatic brain injury prevention in patients with mild cognitive impairment.
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50/100
Dementia, particularly Alzheimer's disease (AD), presents a growing global health challenge characterized by cognitive decline, behavioral changes, and loss of independence.
Why it matters
Machine learning models using UK Biobank health, genetic, and lifestyle data predicted Alzheimer's disease risk with a best ROC-AUC of 0.773, with ApoE-ε4 the most predictive genetic marker and comorbidities, education, physical activity, and diet among key non-genetic predictors. This is risk prediction and does not show that any intervention prevents or treats Alzheimer's disease.
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We identified 471 proteins with significant interaction effects between T2D and dementia risk.
Why it matters
This large-scale proteomic analysis identified 471 proteins with significant interaction effects between type 2 diabetes and dementia risk, and a 51-protein model predicted 15-year dementia risk in people with type 2 diabetes with an AUC of 0.835. The authors say the identified pathways suggest potential therapeutic targets, but this is a risk-stratification and target-identification study, not a tested treatment or cure.
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.
- ATP-binding cassette transporter A7 (ABCA7) loss of function alters Alzheimer amyloid processing
- Alzheimer's Disease: The Amyloid Cascade Hypothesis
- Efficacy of Group Reminiscence Therapy on Cognition, Depression, Neuropsychiatric Symptoms, and Activities of Daily Living for Patients With Alzheimer Disease
- Amyloid pathology and axonal injury after brain trauma
- EEG coherence reflects regional corpus callosum area in Alzheimer's disease
- Hierarchical-circular model of biological memory: a multilevel hypothesis for pathogenesis and allostatic integrity in Alzheimer’s disease and related dementias
- Associations between Alzheimer's disease blood biomarkers and neighborhood disadvantage: A HABS-HD community cohort study
- Development of cognitive instruments for use in clinical trials of antidementia drugs: additions to the Alzheimer's Disease Assessment Scale that broaden its scope. The Alzheimer's Disease Cooperative Study
- The role of cortical connectivity in Alzheimer's disease pathogenesis: a review and model system
- Vascular dysfunction in the pathogenesis of Alzheimer's disease--A review of endothelium-mediated mechanisms and ensuing vicious circles