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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Compared with no testing, the CSF strategy yielded 0.011 additional life-years and 0.019 additional QALYs for an extra cost of THB2,589 (USD71), resulting in an ICER of THB132,961 (USD3,632) per QALY.
Why it matters
This modeling study in Thailand found that cerebrospinal fluid biomarker testing for early detection of Alzheimer's disease and mild cognitive impairment yielded 0.019 additional quality-adjusted life-years compared with no testing, at an extra cost of THB2,589. It does not test a treatment or cure, but it suggests CSF testing may be cost-effective in that setting, with the caveat that further local epidemiological studies could refine the results.
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Comparison of proteins between the three groups revealed significantly lower Aβ1-42, higher Tau and pTau protein expression in serum of patients with Alzheimer disease as compared to patients with mild cognitive impairment and controls.
Why it matters
In this follow-up study, people with Alzheimer's disease had lower serum Aβ1-42 and higher Tau and pTau than those with mild cognitive impairment and controls, and those who progressed showed falling Aβ1-42 and rising Tau and pTau over one year. It does not test a treatment or cure, but it suggests these blood proteins may help track diagnosis and progression.
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To investigate alterations in resting-state electroencephalogram (EEG) microstates across the cognitive spectrum of Parkinson's disease (PD) and to evaluate their utility as electrophysiological biomarkers of cognitive impairment.
Why it matters
This study found that specific EEG microstate patterns differ between Parkinson's disease patients with and without dementia, and these patterns correlate with cognitive test scores. These findings could help identify cognitive decline in Parkinson's disease, but the study does not test any treatment or prevention.
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Plain Language SummaryWhat is this summary about?
Why it matters
This plain language summary reports that brexpiprazole reduced agitation in almost all groups of people with Alzheimer's dementia compared to placebo, with no clear differences in side effects across groups. It addresses a treatment for agitation, a symptom of the disease, rather than a cure or prevention.
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Lecanemab is a humanized IgG1 monoclonal antibody binding with high affinity to protofibrils of amyloid-beta (Aβ) protein.
Why it matters
Modeling of lecanemab trial data found that amyloid PET reduction predicted drug effect better than drug exposure, and projected growing differences in CDR-SB over 4 years. This supports amyloid reduction as a marker of efficacy for lecanemab but does not establish a cure or prevention.
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Random Forest achieves the highest accuracy of 97% on clinical data, while CNN achieves the best overall performance of 94% in MRI-based staging.
Why it matters
This study reports that a Random Forest model reached 97% accuracy on clinical data and a CNN reached 94% in MRI-based staging of Alzheimer's disease, with interpretable AI highlighting hippocampal atrophy and ventricular enlargement. It is a diagnostic study and does not test any treatment, cure or prevention.
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Within the limitations of measuring in vitro equilibrium binding activity of in‐house recombinant antibodies to aqueously extracted Aβ from human postmortem brain tissue, we could not discern a population of Aβ aggregates ( e.g . protofibrils) accessible to one antibody but not the other two.
Why it matters
This laboratory study found that lecanemab, aducanumab, and donanemab bind the same human Alzheimer's Aβ aggregates at different sites, and that lecanemab did not prefer soluble Aβ over aducanumab. It also found that aducanumab, which causes the most ARIA, did not consistently prefer cerebral amyloid angiopathy Aβ, so it does not explain why these antibodies cause ARIA at different rates.
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The ABC-DS cohort showed similar Aβ PET burden but had a lower prevalence of ApoE4 carriers, younger age at clinical diagnosis and autopsy, shorter PET-autopsy interval, smaller amygdala and hippocampal volumes, more advanced CERAD scores, and no atherosclerosis compared to ADRC cohort (Figure 1).
Why it matters
In the Down syndrome cohort, antemortem amyloid PET burden was associated with advanced LATE-NC stage but not with postmortem amygdala or hippocampal volumes, and no significant associations were found for Thal phase, Braak NFT stage or CERAD score. These correlational autopsy findings do not show how to treat, cure or prevent Alzheimer's disease.
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MOLDI-MS identified eighty-five proteins represented by multiple tryptic peptides, twenty-five of which showed significant differences between DS and controls, confirmed by WB and ELISA analysis.
Why it matters
This study identified 25 serum proteins that differed significantly between people with Down syndrome and controls, some of which have been linked to Alzheimer disease risk pathways. The authors suggest these proteins may be developed into non-invasive markers, but no treatment, cure or prevention is tested.
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Alzheimer's disease (AD) is often underdiagnosed, especially at early stages when symptoms are mild, and patients may benefit from new and recently approved anti-amyloid therapies.
Why it matters
This paper presents an Early Alzheimer's Disease Patient Care Pathway as an implementation guide covering identification, assessment, diagnosis, treatment, and monitoring. It is a framework for care delivery and does not report new evidence on treating, curing, or preventing the disease.
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The four- and seven-class clustering solutions achieved high variance overlap with published microstate templates.
Why it matters
This study found that EEG microstate parameters differentiated patients with dementia from healthy controls and were associated with MMSE scores. Ratio-normalized parameters improved group discrimination.
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Herpes simplex virus type 1 (HSV-1) is a continuous health challenge, and current antiviral treatments cannot cure the virus.
Why it matters
This review assesses evidence linking HSV-1 to Alzheimer's disease through chronic neuroinflammation, amyloid-beta and tau accumulation, oxidative stress and synaptic dysfunction, and notes that antivirals reduce symptoms but do not eradicate the virus. It outlines experimental models needed to establish causality, so no antiviral is yet shown to prevent or treat Alzheimer's.
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Among 1,706 participants (mean age 56 years, 62% female, 28% Black), midlife NAFLD vs no NAFLD was associated with greater late-life WMH volume (difference per SD 0.19, 95% CI 0.06-0.31) and faster late-life WMH increase over 6 years (difference in annual change, SD 0.28, 95% CI 0.05-0.51), suggesting accumulating vascular pathology.
Why it matters
In 1,706 participants, midlife nonalcoholic fatty liver disease was linked to greater late-life white matter hyperintensity volume and faster increase over six years, as well as to Alzheimer's blood and imaging markers in midlife and late life. The authors say this reveals potential pathways linking liver function to dementia and that plasma biomarkers may help monitor the effects of impaired liver function on brain health.
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36/100
This study aims to investigate the syntactic complexity in individuals with Alzheimer's disease (AD) by conducting a comprehensive analysis that incorporates mean dependency distance (MDD), fine-grained grammatical metrics, and dependency network structures.
Why it matters
This study found that people with Alzheimer's disease shifted from complex clause-based sentence structures to simpler phrase-based ones, which the authors link to working memory deficits. These findings describe a language pattern in Alzheimer's disease and do not address treating, curing, or preventing it.
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Physical inactivity and low fitness have become global health concerns.
Why it matters
This study combined machine learning and metabolic network analysis to identify metabolite biomarkers linked to fitness in elderly individuals, with aspartate emerging as a dominant marker. It is about understanding active aging and metabolism, not treating, curing or preventing Alzheimer's disease.
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PFT is longer at CDR-SB ≤ 2.0 (1-2 years) and shorter at CDR-SB ≥ 5 (≤ 0.33) in the Alzheimer's Disease Neuroimaging Initiative cohort.
Why it matters
This study estimated progression-free time at each 0.5-unit step of the CDR-SB in inherited and sporadic Alzheimer's disease and used it to estimate that three years of continuous lecanemab treatment delays progression by 0.62 years in the sporadic population. The authors say the measure needs further validation before it can serve as a benchmark for clinical progression and treatment effects.
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In the whole sample, both PRSs were associated with the strength of correlation between GMV and different serotonin receptors and fluorodopa uptake.
Why it matters
In ADNI participants, brain atrophy was negatively associated with serotoninergic and dopaminergic receptors/transporters, and AD polygenic risk scores were associated with the strength of these correlations. This explores genetic and neurotransmitter links to atrophy, not any treatment, cure, or prevention.
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Research revealed a significant locus of susceptibility for LOAD on the Bridging Integrator 1 (BIN1) that is situated on chromosome 2q14.3 and is identified at the time of the most significant susceptibility gene of LOAD.
Why it matters
This review describes BIN1 as a susceptibility gene for late-onset Alzheimer disease, with a shift in BIN1 isoform expression in the disease. It reports no treatment, cure, or prevention results.
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Alzheimer's disease (AD) is a neurodegenerative disorder characterized by a set of multifactorial conditions that progressively impair memory processing and cognitive function.
Why it matters
This review summarizes evidence on cannabidiol in Alzheimer's disease and uses computer-based analysis of gene networks and pathways. It is not a clinical trial, so it does not show that cannabidiol treats or prevents Alzheimer's disease in people.
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About one billion people worldwide are affected by neurologic disorders.
Why it matters
This in silico transcriptomic analysis found dysregulation of RNA splicing and translation processes in blood samples from people with mild cognitive impairment and Alzheimer's disease. As a computational analysis of existing data, it suggests possible markers but does not test any treatment, cure, or prevention.
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Why it matters
This is a comment by European Alzheimer's Disease Consortium investigators on the negative recommendation of the CHMP regarding marketing authorization of donanemab for early Alzheimer's disease. The available text contains no findings on treating, curing or preventing the disease.
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Alzheimer's disease (AD) is a neurodegenerative disease, representing the seventh cause of death worldwide and the first cause of dementia.
Why it matters
This minireview suggests that exposure to arsenic, among other heavy metals, may be linked to Alzheimer's disease and may induce DNA hypomethylation in the brain through mechanisms not yet fully understood. It presents a hypothesis about environmental risk, not a treatment, cure or prevention.
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The findings indicate that the burden of dementia is rising in East and Southeast Asia, with women showing a higher burden across all indicators.
Why it matters
This study found that dementia burden is rising in East and Southeast Asia, with women bearing a higher burden, and identified smoking, high blood sugar, and high body mass index as important risk factors. The findings highlight the need for region-specific approaches to allocate healthcare resources and control measures.
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36/100
Rats in the AD and AD + P groups performed worse in behavioral tests compared to controls (p 0.05).
Why it matters
In rats, periodontitis worsened Alzheimer's-like molecular pathology, particularly tau hyperphosphorylation, while periodontal treatment reduced NF-kβ levels and improved behavioral outcomes. This is animal research, so it does not establish that treating gum disease affects Alzheimer's disease in people.
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It is often associated with recurrent ICH, seizures, and cognitive impairment.
Why it matters
This opinion paper describes iatrogenic cerebral amyloid angiopathy as a documented condition that may arise from prior exposure to cadaveric materials such as lyophilized dural grafts used in neurosurgery, often appearing 30 to 40 years later. It argues for increased clinical awareness and for reassessing surgical practices to reduce this preventable condition.
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.
- Evaluation of a panel of plasma biomarkers for Alzheimer's disease in a diverse research cohort
- [Diagnosing Alzheimer Dementia in People with Down Syndrome in Accordance with ICD, DSM V and A/T/N System]
- Plasma biomarkers identify brain ATN abnormalities in a dementia-free population-based cohort
- Shared genetic architecture between brain iron deposition and Alzheimer's disease
- The efficacy of Ginkgo biloba on cognitive function in Alzheimer disease
- Regional distribution of white matter hyperintensities in vascular dementia, Alzheimer's disease and healthy aging
- Amyloid imaging of Lewy body-associated disorders
- Classification of Alzheimer's Disease with Respect to Physiological Aging with Innovative EEG Biomarkers in a Machine Learning Implementation
- Parallel electrophysiological abnormalities due to COVID-19 infection and to Alzheimer's disease and related dementia
- Machine learning reveals distinct neuroanatomical signatures of cardiovascular and metabolic diseases in cognitively unimpaired individuals