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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Significant interactions between amyloid status and modifiable risk factors were observed for diabetes (adjusted β = -0.206, p = 0.032), high cholesterol (adjusted β = -0.155, p < 0.001), and physical inactivity (adjusted β = -0.161, p = 0.046), indicating combined effects rather than additive effects on cognitive decline among Aβ+ individuals.
Why it matters
In this cohort study, diabetes, high cholesterol, and physical inactivity were associated with faster cognitive decline specifically in amyloid-positive individuals, suggesting combined rather than additive effects. In amyloid-negative participants these associations were not statistically significant, and the authors say future studies should assess whether modifying these factors changes outcomes.
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To efficiently implement plasma and cerebrospinal fluid (CSF) biomarkers for staging and prognosis of Alzheimer disease (AD), we must understand their dynamics across disease progression.
Why it matters
This study found that %p-tau217 changes earliest in the disease process, just before amyloid PET becomes positive, while other tau markers change later and MTBR-tau243 tracks cortical tau burden in later stages. The authors say measuring these markers together provides information about different biological events in the disease cascade, which could benefit clinical trials and patient management.
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Pathophysiologic-constrained ADL provided interpretable, personalized pathologic maps and an AI-derived ADAD score that more closely linked PET pathologic abnormalities with multimodal clinical measures. © RSNA, 2026
Why it matters
This study developed a deep-learning method to separate Alzheimer's-related amyloid and tau abnormalities from normal brain uptake on PET scans, creating a score that may better match clinical findings. It is a diagnostic and monitoring tool and does not test any treatment, cure, or prevention.
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Accurate prediction of progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD) is critical for early intervention.
Why it matters
This study found that higher scores on ADAS-Cog13, ADAS-Cog11, CDR-SB, and FAQ increased the hazard of conversion from mild cognitive impairment to Alzheimer's disease, while higher RAVLT-IR, RAVLT-L, and MMSE scores were protective, and APOE-ε4 carriage was a consistent risk factor. It does not test a treatment or cure, but it suggests certain cognitive measures may help predict who will convert.
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In this real-world dataset, we identified effects of multimorbidities on plasma biomarkers, especially kidney function.
Why it matters
In a real-world diverse clinical population, the ratio of plasma p-tau217 to Aβ42 was most strongly linked to Alzheimer's-related factors, but it was also linked to kidney function, diabetes and hearing loss. This shows that other medical conditions can affect how these blood biomarkers should be interpreted; it is not a treatment.
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TabCAT tests showed good convergent validity with traditional pen-and-paper tests.
Why it matters
This multisite study found that tablet-based cognitive tests correlated with traditional pen-and-paper tests and were associated with amyloid and tau PET patterns in early-onset Alzheimer's disease. It is about digital cognitive assessment for identification, not treatment or cure.
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α-Synuclein (αSyn) seed amplification assays (SAAs) accurately detect αSyn pathology in dementia with Lewy bodies (DLB).
Why it matters
This study looked at how different alpha-synuclein seed amplification assay and Alzheimer's biomarker profiles relate to presentation and progression in dementia with Lewy bodies. It aims to help prognosis and clinical trial design, not to treat, cure or prevent Alzheimer's disease.
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The complexity of neurodegenerative disorders necessitates an integrative approach that incorporates morphological, functional, and molecular biomarkers.
Why it matters
In this cohort, blood-based biomarkers including NfL, GFAP and p-tau181 helped distinguish between neurodegenerative conditions such as Alzheimer's disease, Parkinson's disease and atypical parkinsonisms. The study evaluates diagnostic utility only and reports no treatment or cure.
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53/100
In the Rush dataset, we included 1,277 women and 579 men.
Why it matters
This study found sex differences in associations of Lewy body disease with Alzheimer's disease pathologies and cognitive decline, with men showing faster LBD-related decline and women faster neurofibrillary tangle-related decline. It highlights the need for precision approaches to dementia prevention and intervention, but no specific treatment is provided.
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In contrast, patients with LB pathology alone, in the absence of AD biomarker positivity, had less overall cognitive impairment but more focal dysexecutive and visuospatial deficits.
Why it matters
This paper discusses how co-pathologies such as Lewy body and TDP-43 pathology alter the disease course in Alzheimer's disease and dementia with Lewy bodies, being associated with more aggressive disease and poorer cognition. It describes the importance of co-pathologies for understanding disease progression but does not test any treatment, cure or prevention.
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We show that semaglutide was associated with a significantly reduced risk of overall ADRD incidence with a hazard ratio ranging from 0.54 (0.49-0.59) compared with insulin, 0.67 (0.61-0.74) compared with metformin, to 0.80 (0.72-0.89) compared with older generation glucagon-like peptide-1 agonists (GLP-1RAs).
Why it matters
In patients with type 2 diabetes, semaglutide was associated with a lower risk of Alzheimer's disease and related dementias compared with insulin, metformin, or older GLP-1 agonists, with reduced risk specifically for vascular dementia. The study calls for randomized trials to establish causality and understand mechanisms.
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Greater intra-group heterogeneity in ATN abnormality patterns was observed in more severe clinical stages of AD.
Why it matters
This study found that abnormalities in amyloid, tau, and neurodegeneration imaging markers were more varied among patients at more severe stages of Alzheimer's disease. A patient-specific measure of these abnormalities was linked to worse cognitive function and increased risk of disease progression.
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53/100
Amyloid burden is an important prognostic marker in a clinically heterogeneous cohort.
Why it matters
In a heterogeneous cohort, amyloid PET positivity predicted progression from unimpaired to mild cognitive impairment and dementia and was linked to faster decline in memory, language, and other functions. This supports amyloid PET as a prognostic marker, but does not show any treatment, cure, or prevention.
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Alzheimer's disease (AD), the leading cause of dementia, is characterized by the accumulation of amyloid plaques and neurofibrillary tangles in the brain.
Why it matters
This review describes Alzheimer's disease as complex and multifactorial, influenced by genetic predispositions and risk factors including aging, systemic inflammation, chronic health conditions, lifestyle, and environmental exposures. It says recent advances are paving the way for improved diagnosis, risk assessment, and potentially effective prevention strategies, but no specific treatment or cure is reported.
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These pathological changes lead to widespread neuronal damage, significantly impacting daily functioning and quality of life.
Why it matters
This review states that Alzheimer's disease is influenced by genetic factors such as APOE ε4 and by modifiable factors like diet, physical activity, and cognitive engagement. It concludes that ongoing research is needed to find new therapeutic targets and improve diagnosis and treatment.
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MR analysis suggested a causal relationship between decreased blood-derived mtDNA-CN and increased risk of AD (OR = 0.68; P = 0.013).
Why it matters
Genetic analysis suggested that lower blood-derived mitochondrial DNA copy number is causally linked to higher Alzheimer disease risk and to conversion from mild cognitive impairment to Alzheimer disease. This points to mitochondrial function as a possible risk pathway, but it does not show that changing mitochondrial DNA copy number prevents or treats the disease.
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53/100
Alzheimer's disease (AD) is the most common cause of dementia and accounts for 60-70 % of all cases.
Why it matters
This is a review of what is known about how Alzheimer's disease develops, how it is diagnosed, and what treatments are being explored. It reports no new treatment or cure and presents no results from a trial.
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Of 108 participants (age: 69 ± 6.5 years; 54.6% female) with paired samples obtained at time of LP, 64.8% (n = 70/108) had Aβ pathology detected (35 with Mild Cognitive Impairment and 35 with mild dementia).
Why it matters
In 108 people attending a memory clinic, a blood test for p-tau217 distinguished those with amyloid pathology from those without with excellent performance. This supports blood testing as a way to detect Alzheimer's-related amyloid, but it does not itself treat, cure or prevent the disease.
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53/100
Alzheimer's disease (AD) accounts for 60-70% of the population with dementia.
Why it matters
This study developed a machine learning model to predict conversion from mild cognitive impairment to Alzheimer's disease using imaging and demographic features. It does not test any treatment, cure, or prevention, and it suggests the model could be useful for early diagnosis and treatment planning.
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ARIA monitoring is important to inform treatment dosing decisions and might be improved through assistive software.
Why it matters
This diagnostic study assessed an artificial intelligence-based software tool for assisting radiological interpretation of brain MRI scans in patients monitored for amyloid-related imaging abnormalities (ARIA). It addresses monitoring of a treatment side effect, not treating, curing or preventing Alzheimer's disease itself.
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For amyloid positive individuals Aβ42/Aβ40, glial fibrillary acidic protein and p-tau181 were the top predictors of cognitive decline while Aβ42/Aβ40 was prominent for amyloid negative participants across all age groups.
Why it matters
This study tested whether combining Alzheimer's plasma biomarkers with MRI, cardiovascular, genetic, and lifestyle measures improves prediction of cognition. It concerns prediction, not treating, curing, or preventing Alzheimer's disease.
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According to the World Health Organization (WHO), dementia is the seventh leading reason of death among all illnesses and one of the leading causes of disability among the world's elderly people.
Why it matters
This study combined clinical, MRI, and psychological data with machine learning to classify five categories including Alzheimer's disease, reporting 98.81% accuracy with a Random Forest classifier. It is about improving diagnosis, not about treating, curing, or preventing Alzheimer's disease.
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Recent studies show that Alzheimer's disease (AD) has many common links with conditions associated with insulin resistance, including neuroinflammation, impaired insulin signaling, oxidative stress, mitochondrial dysfunction and metabolic syndrome.
Why it matters
This review looks at diabetes drugs as possible Alzheimer's treatments, since the two conditions share problems such as insulin resistance and inflammation. Metformin, intranasal insulin, thiazolidinediones and incretins showed positive effects in both people and animal models, but rosiglitazone may carry a significant risk of side effects. Clinical results for metformin in Alzheimer's were limited and contradictory, so the case is not settled.
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Evidence shows that ADAM10 levels are altered in platelets, plasma, serum, and CSF of individuals with AD.
Why it matters
This systematic review of 17 studies looked at ADAM10, an enzyme that steers amyloid precursor protein away from making amyloid-β, as a possible Alzheimer's biomarker. ADAM10 was consistently lower in platelets but higher in plasma of people with Alzheimer's, while spinal fluid results conflicted, possibly due to differing lab methods. The authors see it as a possible complementary biomarker but say cut-off values still need to be established.
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53/100
A location dynamics model and ADRD-focused future directions are offered for guiding rural practitioners, researchers, and policymakers in mitigating rural disparities.
Why it matters
This review reports that people in rural communities face heightened risk and burden from Alzheimer's disease and related dementias, and identifies individual, interpersonal and community factors. It offers a location dynamics model and future directions for reducing these disparities, rather than testing a 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.
- Neuropathology of dementia in patients with Parkinson's disease: a systematic review of autopsy studies
- Clinical and biomarker changes of Alzheimer's disease in adults with Down syndrome: a cross-sectional study
- Sex Differences in the Associations of Obesity with Tau, Amyloid PET, and Cognitive Outcomes in Preclinical Alzheimer's Disease: Cross-Sectional A4 Study
- Does the Female Advantage in Verbal Memory Contribute to Underestimating Alzheimer's Disease Pathology in Women versus Men?
- Brain and blood metabolite signatures of pathology and progression in Alzheimer disease: A targeted metabolomics study
- Cerebrospinal fluid dynamics disorders: Relationship to Alzheimer biomarkers and cognition
- Safety, Tolerability, and Feasibility of Young Plasma Infusion in the Plasma for Alzheimer Symptom Amelioration Study: A Randomized Clinical Trial
- Trends in Alzheimer Disease Mortality Among American Indian and Alaska Native People Between 2011 and 2019
- APOE and Alzheimer's disease and related dementias risk among 12,221 Hispanics/Latinos
- Blood Ammonia as a Possible Etiological Agent for Alzheimer's Disease