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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Cross-ancestry sex-stratified analyses identified several loci with evidence of interaction (p 0.05).
Why it matters
This large genetic analysis identified several sex-specific genetic loci associated with Alzheimer disease, including some found only in females or only in males. These findings may help explain sex differences in Alzheimer risk, but they do not yet provide a treatment or prevention.
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In ARIC (n = 1,736, mean age 63, 58.8% female, 48.7% non-Hispanic White individuals, median follow-up 18.6 years), the dementia incidence rate was 10.4 (95% CI, 9.2-11.6) per 1,000 person-years.
Why it matters
In two large longitudinal cohorts, white matter hyperintensity burden and APOE ε4 status each increased dementia risk, and having both raised risk further. The authors say these findings support the potential benefit of vascular risk management to reduce white matter hyperintensities and delay dementia onset, even in people genetically at risk.
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No adverse events occurred over the study period.
Why it matters
In this small pilot of five people with mild Alzheimer's disease, daily 40 Hz audiovisual stimulation for two years caused no adverse events, and three patients with late-onset disease showed less decline on cognitive scores than matched controls. The authors describe this as a small early study supporting further investigation, not proof of benefit.
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57/100
Subjective cognitive decline (SCD) may be an early indicator of Alzheimer disease and related dementias (ADRD), yet its association with plasma biomarkers remains unclear among middle-aged and older adults (aged 50-86 years).
Why it matters
This cross-sectional study examined associations between several plasma biomarkers and subjective cognitive decline in middle-aged and older Hispanic and/or Latino adults. It is about biomarker associations with a self-reported symptom, not about treating, curing or preventing Alzheimer's disease.
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Personalized repetitive transcranial magnetic stimulation (rTMS) of the precuneus (PC) is emerging as a new non-invasive therapeutic approach in treating Alzheimer’s disease (AD).
Why it matters
In this randomized trial, 52 weeks of personalized repetitive transcranial magnetic stimulation over the precuneus significantly affected the primary outcome and several secondary outcomes in people with mild-to-moderate Alzheimer's disease. Stronger connectivity in a brain network at baseline was linked to better response to the treatment.
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In the context of global ageing, the prevalence of neurodegenerative diseases and dementia, such as Alzheimer's disease (AD), is increasing.
Why it matters
This review argues that ageing is the primary risk factor for neurodegenerative diseases and proposes that prevention and treatment should be based on holistic antiageing approaches alongside interventions targeting disease-specific events. It offers a perspective rather than testing any specific treatment, so it does not show that any antiageing strategy works in people.
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Meta-analysis identified 44 CpGs and 44 differentially methylated regions consistently associated with time to dementia in both cohorts.
Why it matters
A blood DNA methylation signature was consistently associated with time to dementia across two cohorts, and a methylation-based risk score predicted future cognitive decline in an independent validation set even after accounting for other factors. The authors describe DNA methylation as a promising source for dementia risk assessment.
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57/100
We present a comprehensive global analysis of genetic variants associated with autosomal-dominant Alzheimer's disease (ADAD).
Why it matters
This global analysis identified 550 variants in APP, PSEN1 and PSEN2 associated with autosomal-dominant Alzheimer's disease, classified 279 as pathogenic or likely pathogenic, and estimated age at onset for 227 variants. It also found that mean variant age at onset and parental age at onset help predict symptomatic onset, which may refine eligibility for disease-modifying clinical trials, but the study itself does not test a treatment or cure.
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Bariatric surgery was associated with a significantly reduced incidence of ADRD, evidenced by a subdistribution hazard ratio (SHR) of 0.37 (95% confidence interval [CI]: 0.15–0.89; P = 0.03).
Why it matters
In this retrospective cohort, bariatric surgery was associated with significantly reduced incidence of Alzheimer disease and related dementias and mild cognitive impairment, and with a delay of about two years before developing MCI. These findings suggest bariatric surgery may serve as an effective strategy to delay MCI onset and reduce dementia risk in patients with obesity.
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Analyses revealed significant nonlinear interaction effects of ELS severity and age on NfL and GFAP serum concentrations, total and subcortical gray matter volume loss, increased third ventricular volume, and cognitive impairment.
Why it matters
In women, greater early-life adversity was linked with markers of neuroinflammation, neurodegeneration, brain volume loss, and cognitive impairment as they aged. The authors say these findings could inform early prevention strategies, but no treatment or prevention method is tested here.
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57/100
We discovered a remarkable gender-specific difference in DEGs that distinguish P-MCI from S-MCI.
Why it matters
Blood-based transcriptomic signatures, including an 8-gene signature, distinguished rapidly progressing from slowly progressing mild cognitive impairment with high accuracy. This may help identify high-risk patients, but does not provide a treatment, cure or prevention.
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Alzheimer's disease (AD) is the most common neurodegenerative dementia with multi-layered complexity in its molecular etiology.
Why it matters
This review summarizes over 200 human studies that used large-scale molecular (omics) methods to find Alzheimer's-related changes in the brain's glial cells: microglia, oligodendrocytes, astrocytes and blood vessel cells. It sets out shared and cell-specific changes in each group. The authors discuss what these mean for disease progression and future treatment, but no therapy is tested here.
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This study highlighted that the AD-causal MD genes could be regulated by epigenetic changes and interact with inflammatory cytokines, providing evidence for AD prevention and intervention.
Why it matters
Combining brain gene-expression data with genetic (Mendelian randomization) methods, this study identified mitochondrial-function genes that may play a causal role in Alzheimer's, such as NDUFS8 and SPG7 in blood and CLU and MAPT in brain, and found them influenced by DNA methylation. Some also interacted with inflammatory molecules including interleukin-18. These computational findings suggest targets for prevention and treatment research rather than ready interventions.
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The proposed method offers a fully automated procedure, providing an opportunity to develop an inexpensive, broadly accessible, and easy-to-administer screening tool for MCI-to-AD progression prediction, facilitating development of remote assessment.
Why it matters
This study used speech recordings and machine learning to predict which people with mild cognitive impairment would develop Alzheimer's disease within 6 years, with 78.5% accuracy and 81.1% sensitivity. It suggests a possible low-cost, easy-to-administer screening tool, but it is a prediction method, not a treatment or cure.
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Insulin, insulin-like growth factors (IGF) and their receptors are highly expressed in the adult hippocampus.
Why it matters
This study measured the protein IGFBP2 in cerebrospinal fluid from 109 asymptomatic people with a parent who had Alzheimer's disease, alongside core Alzheimer's and synaptic biomarkers. It is a biomarker study, so it does not show that changing IGFBP2 levels treats, cures or prevents the disease.
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This study revealed that 18 weeks of gum chewing with Olibanum did not change the neuropsychological status.
Why it matters
In 72 people with mild-to-moderate Alzheimer's disease, 18 weeks of olibanum chewing gum did not significantly change neuropsychological status or MMSE scores compared with placebo. This is a clear null result for this treatment.
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57/100
Amyloid PET imaging has been crucial for detecting the accumulation of amyloid beta (Aβ) deposits in the brain and to study Alzheimer's disease (AD).
Why it matters
This large multi-ethnic genetic study identified APOE and several other genetic loci associated with brain amyloidosis and Alzheimer's disease risk, including some female-specific signals. It is a genetic association study and does not report any treatment, cure, or prevention of Alzheimer's disease.
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Our findings suggest that the informant report is particularly relevant in patients with MCI where it strongly relates to higher amyloid-PET, indicative of impairment due to AD.
Why it matters
In 110 participants across the Alzheimer clinical continuum, informant-reported memory decline was especially relevant in people with mild cognitive impairment, where it related strongly to higher amyloid-PET. This supports using informant reports in assessment, not a way to treat or prevent the disease.
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Under Bronfenbrenner's macrosystem framework, we highlight key quantitative and qualitative studies linking S/SDOH with AD/ADRD, identify scientific gaps in the literature, and propose guidance for future research.
Why it matters
This review uses Bronfenbrenner's ecological systems theory to propose how structural and social forces — including racism, classism, sexism and homophobia, and the laws and social norms that carry them — may drive unequal dementia risk and outcomes across a lifetime. The authors say these "macro-level determinants have been understudied" in Alzheimer's research, and they set out gaps and a research agenda. It is a framework that reports no new data, and it does not test whether these factors cause dementia.
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Alzheimer's disease (AD) pathologies were discovered in the accessible neurosensory retina.
Why it matters
In this study of postmortem retina and brain tissue from 86 donors, mild cognitive impairment and Alzheimer's disease retinas showed increases in amyloid β-protein forms and intraneuronal Aβ oligomers associated with retinal inflammation and atrophy. These retinal changes correlated with brain measures, but the work is on donated tissue and does not test treatment or prevention.
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Our study indicates that EEG can be used as a useful screening tool for the diagnosis and disease progression evaluation of MCI and AD.
Why it matters
Using EEG recordings from 890 participants, this study identified biomarkers that achieved over 70% accuracy in distinguishing healthy controls, mild cognitive impairment, and Alzheimer's, and combined them with other data to assess progression. The authors conclude EEG can be a useful screening tool for diagnosis and progression, but it is a diagnostic study and no treatment was tested.
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57/100
Higher vascular disease burden increases the likelihood of developing dementia, including Alzheimer's disease.
Why it matters
This study found that diabetes and hypertension were related to amyloid-beta burden in the brain before dementia in a population-based cohort. It reports associations and does not show that treating these conditions prevents or cures Alzheimer's disease.
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Alzheimer's disease (AD) is a chronic neurodegenerative disease characterized by the progressive accumulation of amyloid-beta and neurofibrillary tangles of tau in the neocortex.
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In sum, we present a diagnostic tool for MCI and AD trained using baseline scans and a follow-up diagnosis regardless of progression, which is multi-diagnostic, generalizable across independent data sources and acquisition protocols, and with transparently reported performance.
Why it matters
Machine learning classifiers using structural MRI achieved 90.6% balanced accuracy in distinguishing Alzheimer's disease from healthy controls, with hippocampal features as the strongest contributors. This is a diagnostic tool and does not treat, cure, or prevent Alzheimer's disease.
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Amyloid beta (Aβ) plaque is a defining pathologic feature of Alzheimer disease (AD).
Why it matters
In an 84-year-old woman with Alzheimer's disease who received 32 monthly doses of aducanumab, amyloid PET showed reduced amyloid plaques and autopsy found sparse residual plaques, but neurofibrillary degeneration was still present at Braak stage V. This single case report shows plaque reduction but does not demonstrate that aducanumab stops tau pathology or improves clinical outcomes.
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.
- Obstructive sleep apnea and longitudinal Alzheimer's disease biomarker changes
- Layer-Specific Colocalization of Microglia with Amyloid Plaques in the Middle Temporal Gyrus Predicts Cognitive Decline in Alzheimer's Disease
- The role of nutrition in Alzheimer's disease
- Comment by European Alzheimer’s Disease Consortium (EADC) investigators on the negative recommendation of the CHMP on the marketing authorization of donanemab for early Alzheimer’ s disease
- Amnestic syndrome of the medial temporal type identifies prodromal AD: a longitudinal study
- Sex and Gender Driven Modifiers of Alzheimer's: The Role for Estrogenic Control Across Age, Race, Medical, and Lifestyle Risks
- The E280A presenilin 1 Alzheimer mutation produces increased A beta 42 deposition and severe cerebellar pathology
- Intervention for a Digital, Cognitive, Multi-Domain Alzheimer Risk Velocity Study: Protocol for a Randomized Controlled Trial
- Toward a predictive model of Alzheimer's disease progression using capillary electrophoresis-mass spectrometry metabolomics
- Pathogenic protein seeding in Alzheimer disease and other neurodegenerative disorders