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.
-
Blood-based biomarkers (BBMs) for Alzheimer disease (AD) offer widely expanded access to biomarker-informed diagnoses in community settings that have previously lacked such resources.
Why it matters
This perspective article notes that limited data are available to guide clinicians on when to test for Alzheimer's disease blood-based biomarkers, how to counsel patients with mild cognitive impairment and a positive result about dementia risk, or which prevention strategies or treatments to recommend. It outlines challenges and suggestions for pretest counseling and future research, not a treatment or cure.
-
These findings suggest that circadian rhythm disruption as measured via 24-hour RAR is associated with plasma and imaging biomarkers of AD in DS.
Why it matters
In adults with Down syndrome, more fragmented rest-activity rhythms were associated with higher pTau181 and, in a small subsample, with more amyloid on PET. This is a cross-sectional association and does not show that changing sleep or circadian rhythms would treat, cure or prevent Alzheimer's disease.
-
Among most Latinos in northern Manhattan who learned they had an APOE ε4/ε4 genotype, disclosure did not provoke elevated levels of distress.
Why it matters
This small mixed-methods study of 11 Latino APOE ε4/ε4 homozygotes found that only one participant showed signs of elevated psychological distress after learning their genotype and risk estimate. It concerns the psychosocial impact of risk disclosure and reports no treatment, cure, or prevention findings.
-
Systemic inflammatory biomarkers were primarily associated with age/socio-demographic characteristics, remained strikingly stable over time, and were not associated with AD progression.
Why it matters
Systemic inflammatory biomarkers were not associated with Alzheimer's progression, but higher baseline plasma p-tau217 and GFAP, and experiencing delirium, were linked to faster decline. This points to these markers and delirium as things to watch, not to any treatment that changes the disease course.
-
The approval of disease-modifying antiamyloid therapies has expanded the clinical role of amyloid PET beyond diagnostic confirmation to include baseline characterization and longitudinal monitoring of treatment response.
Why it matters
This guide explains how Centiloid scaling standardizes amyloid PET quantification and how it can be used for monitoring treatment response. It is a methodological overview and does not itself test any treatment or prevention.
-
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the most common cause of dementia in the elderly.
Why it matters
This review describes natural products such as curcumin, resveratrol, and cannabidiol that show promise in reducing amyloid-beta aggregation and neuroinflammation in preclinical studies, but their use is limited by poor solubility, instability, and poor brain penetration. Nanotechnology delivery systems are proposed to overcome these barriers, but no effective therapy in people is established.
-
Alzheimer's disease (AD) is a progressive brain disorder that leads to memory loss and a gradual decline in thinking and reasoning abilities.
Why it matters
This study used a support vector machine model to detect and classify Alzheimer's disease from MRI brain scans, reporting 98.16% classification accuracy and better accuracy, sensitivity and specificity than other machine learning models. It is a diagnostic classification tool only and does not test any treatment, cure or prevention.
-
Compared to controls, the AD/VaD patient group had a significantly higher WML volume (p < .001), reduced global CBF (p < .001), greater brain atrophy, and worse ADAS-Cog scores (p < .001).
Why it matters
In this study of patients with Alzheimer's disease and vascular dementia, white matter lesion volume and reduced cerebral blood flow were significant independent predictors of cognitive impairment severity. The model explained 72% of the variance in cognitive scores.
-
Overall, 64% of PlwAD received at least one AD-Rx.
Why it matters
This study found that people with Alzheimer's disease in rural and high-deprivation regions of Germany had lower odds of receiving antidementia medications. It is about access to existing drugs, not about developing or testing a treatment, cure or prevention.
-
Plasma biomarkers showed promising diagnostic performances and potential clinical usefulness in diagnosing dementia.
Why it matters
This study aimed to establish local cut-off values for plasma biomarkers to distinguish Alzheimer from non-Alzheimer groups in a Thai population. It is a validation study of diagnostic thresholds and reports no treatment or prevention outcome.
-
Annotation. Alzheimer’s disease (AD) is the leading cause of dementia in older adults, characterized by the accumulation of pathological proteins – beta-amyloid (Aβ) and hyperphosphorylated tau protein – resulting in neurodegeneration and cognitive impairment.
Why it matters
Monoclonal antibodies can reduce amyloid plaques and tau aggregates and slow cognitive decline, particularly in early stages of Alzheimer disease. However, the clinical efficacy of individual agents remains debated because of conflicting Phase III results and the risk of side effects, notably ARIA.
-
In partial correlations adjusted for age, there was a significant positive association between the cardiovascular composite (r = .156, p = .016) and resistance score; higher cardiovascular composite was associated with greater than expected Aβ for age.
Why it matters
In people with Down syndrome and Alzheimer's disease, a higher cardiovascular risk score was linked to greater amyloid accumulation for age, and hyperlipidemia was linked to a 1.8 times higher likelihood of this. Managing cardiovascular conditions may help delay or prevent Alzheimer's in this group, though the study does not prove cause and effect.
-
We found a positive main effect of CSF Aβ42/40 (p = 0.011) and p-tau181 (p = 0.012) on BC of the Dorsal Attention Network (DAN) (Figure 1).
Why it matters
In cognitively unimpaired individuals, this study found that cerebrospinal fluid Aβ42/40 and p-tau181 were associated with network properties of the dorsal attention network, and that interactions between Aβ42/40 and default mode network metrics related to cognitive changes. The authors suggest network topology may support cognitive resilience and provide potential targets for intervention, but this is an observational study and does not test any treatment or cure.
-
Lecanemab, an anti-amyloid monoclonal antibody, has been approved for treatment of early Alzheimer's disease.
Why it matters
This study characterized real-world use of lecanemab among Medicare Advantage beneficiaries and found slow uptake, with only 43 more new initiators in the final versus first quarter of 2024. It describes treatment use patterns and safety monitoring, not whether lecanemab cures or prevents Alzheimer's disease.
-
Place-based SDoH measures were higher in Black compared to White participants.
Why it matters
Among Black participants, higher scores on place-based social determinants of health measures were linked to higher blood flow variability, lower mean blood flow, and lower cortical thickness, which are biomarkers related to Alzheimer's disease and related dementias. The authors say these measures may partly capture effects of structural racism on brain health and stress the importance of structural interventions, but this is biomarker research, not a treatment or cure.
-
Cerebral amyloid angiopathy (CAA) is a heterogeneous small vessel disease that can occur independently or alongside Alzheimer disease (AD).
Why it matters
This study asked whether spinal fluid biomarkers can distinguish different patterns of cerebral amyloid angiopathy and help assess bleeding risk. It is about diagnosis and risk classification, not about treating or preventing Alzheimer's disease.
-
Alzheimer disease and its clinical variants have characteristic spatial and temporal progression patterns of amyloid and tau driving symptomatology, but the distribution of microglia density, as measured by 18kDa translocator protein (TSPO) PET, is unknown.
Why it matters
This study found that microglia density, measured by TSPO PET, follows the spatial distribution of tau in amyloid-positive individuals and of neurodegeneration in amyloid-negative individuals. The magnitude, location, and timing of elevated microglia density differed across clinical subtypes of Alzheimer's disease.
-
Down syndrome is a condition caused by trisomy of chromosome 21 and is the most common genetic cause of intellectual disability.
Why it matters
In Medicaid claims for 118,539 adults with Down syndrome, those with obstructive sleep apnea claims had 1.08 times the hazard of an Alzheimer dementia claim compared to those without. This is an observational association and does not show that treating sleep apnea prevents dementia.
-
Alzheimer's disease (AD) is a progressive neurodegenerative condition representing the most common cause of dementia and currently affects millions of people worldwide.
Why it matters
This review describes blood-based biomarkers that may allow earlier, less invasive detection, diagnosis and monitoring of Alzheimer's disease than CSF or PET methods. It is a summary of existing evidence, not a new treatment, cure or prevention study.
-
Co-existing neuropathology was frequent, even among individuals without clinical dementia.
Why it matters
This study of brain tissue found that co-existing pathologies are common, that neocortical Lewy body co-pathology is associated with hallucinations regardless of cognitive status, and that Alzheimer's disease co-pathology in Lewy body disease was linked to more neuropsychiatric symptoms only in the full cohort. It clarifies how mixed pathologies relate to symptoms but does not test treatment, cure or prevention.
-
In DLB, plasma concentrations of GFAP and NfL were associated with MTA, GCA-F, and Fazekas scale; and the Aβ42/40 ratio was associated with PA and Fazekas.
Why it matters
In dementia with Lewy bodies, plasma GFAP and NfL were associated with MRI measures of atrophy and cerebrovascular disease, and adding plasma biomarkers raised the specificity of core clinical features for distinguishing DLB from Alzheimer's disease from 68% to 79% while keeping sensitivity at 90%. This is about improving diagnosis, not about treating, curing or preventing the disease.
-
Alzheimer's disease (AD) is a complex and multifactorial neurodegenerative disorder, recognized as the most prevalent form of dementia.
Why it matters
This review describes multi-target drug design as a strategy to target multiple pathological pathways in Alzheimer's disease at once, since traditional single-target drugs have failed to cure, halt, or reverse disease progression. It notes that this approach faces challenges including complex drug design, difficulty crossing the blood-brain barrier, and regulatory hurdles.
-
No significant associations were found between retinal thickness and AD risk (RNFL: odds ratio [OR]IVW = 1.001, 95% confidence interval [CI] = 0.986-1.017, P = 0.883; GCIPL: ORIVW = 1.008, 95% CI = 0.997-1.019, P = 0.172).
Why it matters
This genetic analysis found no evidence of a causal relationship between retinal thickness and Alzheimer's disease risk in either direction. The results do not support using retinal thickness as a causal marker for Alzheimer's disease.
-
To the Editor: With the aging of the population, the prevalence of Alzheimer’s disease (AD) has increased significantly.
Why it matters
This letter compared quantitative susceptibility mapping and voxel-based morphometry in people with Alzheimer's disease and mild cognitive impairment, combined with neuropsychological tests, to evaluate their diagnostic value. It does not test a treatment or cure, and the available text does not report clear findings on diagnosis.
-
Alzheimer research has been driven by genetic findings: from the 1990s until about 2005, by the identification of amyloid precursor protein (APP) and presenilin (PSEN) mutations, leading to the formulation of the amyloid hypothesis, and then from ~2007 by genome-wide studies which have led to the increasing appreciation of the importance of microglial insufficiency in the disease pathogenesis.
Why it matters
This review describes how genetic findings shaped Alzheimer research, from early amyloid-related mutations to later genome-wide studies highlighting microglial insufficiency. It notes that genetic data can help predict high risk so that earlier treatment becomes more practical, but it reports no new 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.
- Argyrophilic Grain Disease: Demographics, Clinical, and Neuropathological Features From a Large Autopsy Study
- The current status, trends, and challenges of Alzheimer’s disease and other dementias in Asia (1990–2036)
- Validation of Plasma Amyloid-β 42/40 for Detecting Alzheimer Disease Amyloid Plaques
- Current practices by Alzheimer's Disease Research Centers to remunerate research participants
- Exploring geographic variations in quinoa grains: Unveiling anti-Alzheimer activity via GC–MS, LC-QTOF-MS/MS, molecular networking, and chemometric analysis
- Gene expression in Alzheimer neocortex as a function of age and pathologic severity
- Classification of Alzheimer disease, mild cognitive impairment, and normal cognitive status with large-scale network analysis based on resting-state functional MR imaging
- Fish consumption, long-chain omega-3 fatty acids and risk of cognitive decline or Alzheimer disease: a complex association
- From clinical judgment to biology: a clinician's opinion on the use of blood-based biomarkers in Alzheimer's disease
- Implications of sleep disturbance and inflammation for Alzheimer's disease dementia