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 5,413 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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However, a recent systematic review and meta-analysis did not support differences in orexin-A between AD and controls.
Why it matters
This study tested whether spinal fluid orexin-A relates to Alzheimer's biomarkers and cognitive performance in older adults with and without symptomatic disease. It is an observational biomarker study and does not test any treatment.
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This study provides a comprehensive review of the last 10 years of research on neuroinflammation and AD, including the number and impact of research findings, research hotspots, and future trends.
Why it matters
This bibliometric analysis mapped 3,833 publications on brain inflammation and Alzheimer's from 2014 to 2024, finding most came from the United States and China. Research hotspots centered on microglia, the brain's immune cells, mouse models, oxidative stress and amyloid-beta, with the blood-brain barrier and tau protein gaining attention recently. It describes research trends rather than new findings, pointing to calming microglia's inflammatory responses as a direction for future work.
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We aim to investigate the relationships between the population characteristics of patients with Alzheimer's Disease (AD) and their Healthcare Utilization (HU) during the COVID-19 pandemic.
Why it matters
This study examined characteristics of older adults with Alzheimer's disease who were hospitalized during the COVID-19 pandemic. It reports factors associated with longer stays and higher hospitalization frequency, and does not test any treatment, cure, or prevention.
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The evaluation of blood biomarkers on an automated platform exhibited high diagnostic accuracy for AD pathophysiology, and pTau 217 showed excellent diagnostic accuracy to identify participants with AD in a consecutive sample representing the routine clinical practice in a specialized memory unit.
Why it matters
In plasma samples from people in a memory clinic, pTau217 and pTau181 were higher and the Aβ42/40 ratio lower in those with amyloid positivity on CSF testing. This concerns a blood test for detecting brain amyloidosis, not treating, curing or preventing Alzheimer disease.
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Research evidence indicating common metabolic mechanisms through which type 2 diabetes mellitus (T2DM) increases risk of late-onset Alzheimer's dementia (LOAD) has accumulated over recent decades.
Why it matters
This review looked for shared biology between type 2 diabetes and late-onset Alzheimer's, evaluating 923 publications and pulling out 138 gene loci as possible shared risk links. The overlap centred on insulin signalling, inflammation, energy and fat metabolism, and the cell's waste-disposal (autophagy) pathways. The authors say this points to an interplay between brain insulin resistance and inflammation, and should help design more focused long-term studies.
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This comprehensive analysis demonstrated that the variance in AD blood biomarker concentrations was mainly explained by age, with minor contributions from cognition, brain atrophy, and genetics, conversely to CSF measures.
Why it matters
This analysis found that age explained most of the variation in Alzheimer's blood biomarker levels, with only minor contributions from cognition, brain atrophy, and genetics. The authors conclude that blood biomarkers should not be used as stand-alone tests, and the study does not address treatment, cure, or prevention.
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58/100
A diverse and stable microbiota promotes a healthy state, nevertheless, an imbalance in gut or oral bacterial composition, called dysbiosis, can cause gastrointestinal disorders, systemic inflammatory states and oxidative stress, among others.
Why it matters
This review examines how an imbalance in gut or mouth bacteria may feed the brain inflammation seen in Alzheimer's. It describes a leaky gut barrier letting bacterial products into the blood and activating immune cells in the brain, and notes that the mouth bacterium Porphyromonas gingivalis in the brain can increase inflammation and beta-amyloid build-up. It summarizes proposed mechanisms rather than testing any treatment.
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Disease-modifying drug use necessitates better Alzheimer disease (AD) detection.
Why it matters
This 4-year biomarker study in ADNI and MEMENTO examined whether adding mild behavioral impairment to mild cognitive impairment better identifies Alzheimer's disease using CSF biomarkers. It is an observational detection study and does not test any treatment, cure, or prevention.
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This randomized controlled trial aims to investigate the effect of 12 weeks of therapeutic exercise on cognitive function and daily activities in patients with mild Alzheimer's disease (AD).
Why it matters
In people with mild Alzheimer disease, 12 weeks of aerobic plus resistance exercise or resistance exercise alone improved cognitive function and daily activities compared with no exercise. There was no significant difference between the two exercise groups.
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While plasma biomarkers for Alzheimer's disease (AD) are increasingly being evaluated for clinical diagnosis and prognosis, few population-based autopsy studies have evaluated their utility in the context of predicting neuropathological changes.
Why it matters
In a population-based study of 350 participants with autopsy and antemortem plasma testing, Alzheimer's disease neuropathologic change was best predicted by plasma GFAP, NfL, and p-tau181 along with APOE ε4 carrier status and a cognitive score, with a cross-validated AUC of 0.798. GFAP and p-tau provided non-overlapping information on neuritic plaque and Braak stage scores while Aβ42/40 and NfL were mainly useful for predicting neuritic plaque scores, but this concerns prediction of pathology rather than treatment, cure, or prevention.
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58/100
Alzheimer's disease (AD) is a complex multifactorial neurodegenerative disorder and the most common form of dementia.
Why it matters
This review reports that Alzheimer's disease is highly heritable, with heritability estimated at about 70% from twin studies, and that larger genetic studies have greatly increased the number of known disease susceptibility loci. It does not describe a treatment or cure; it indicates that genetic research is expanding knowledge of who may be at risk and why.
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The MIND and Mediterranean diets are associated with less postmortem AD pathology, primarily β-amyloid load.
Why it matters
In 581 autopsied participants, higher MIND and Mediterranean dietary pattern scores were associated with lower global Alzheimer's disease pathology. This is an observational association in older adults and does not prove that these diets prevent or treat Alzheimer's disease.
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Our results support the positive cognitive effects of boswellic acids by reducing the systemic inflammation.
Why it matters
In a 6-month double-blind trial of 85 people with mild to moderate Alzheimer's disease, those given boswellic acids (K-Vie, the main ingredient in Memowell) improved by 3.1 units on the MMSE and 1.6 units on the CDR-SOB compared with placebo, and had lower levels of inflammatory signals such as IL-6 and TNF. Only mild stomach side effects were reported in a few patients. The authors say this supports a cognitive benefit tied to reducing body-wide inflammation, based on this one trial of 85 patients.
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ALPS-index may provide useful disease progression or treatment biomarkers for patients with AD as an indicator of modulation of glymphatic activity.
Why it matters
In 50 participants, a measure of glymphatic system activity correlated negatively with amyloid and tau deposition on PET and positively with cognitive scores. The authors note this is an association and suggest the measure could serve as a progression or treatment biomarker, but the study does not show that altering glymphatic activity treats or prevents Alzheimer's.
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The proposed novel, pragmatic method to determine CSF biomarker cutoffs for AD does not require assessment of other biomarkers or assumptions concerning the clinical diagnosis of patients.
Why it matters
A new method for setting cutoff values for Alzheimer's spinal fluid biomarkers agreed closely with amyloid and tau PET imaging in one study group and was then applied to 10 large patient groups. This is a way to standardize diagnosis, not a treatment, cure or prevention.
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Well-authenticated biomarkers can provide critical insights into the biological basis of Alzheimer disease (AD) to enable timely and accurate diagnosis, estimate future burden and support therapeutic trials.
Why it matters
This review describes blood p-tau biomarkers as possible first-line diagnostic and prognostic tools that could allow wider population screening outside specialised centres. It discusses diagnostic and research use, not a treatment, cure or prevention.
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The ε4 allele of the apolipoprotein E gene (APOE4) is a strong genetic risk factor for Alzheimer's disease (AD) and several other neurodegenerative conditions, including Lewy body dementia (LBD).
Why it matters
This paper proposes an 'ApoE Cascade Hypothesis' in which the biochemical properties of apoE set off a cascade of cellular and systems events that lead to Alzheimer's disease and age-related cognitive decline. It predicts that apoE-targeted therapies may be more effective if aimed at the early biochemical phase, but this is a hypothesis, not a tested treatment or cure.
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58/100
Longitudinal racial differences in amyloid biomarkers are observed.
Why it matters
Among 179 Black and 1,180 White cognitively normal adults, amyloid biomarkers declined or accumulated more slowly in Black participants, and CSF total tau and phosphorylated tau181 increased about half as much. This is an observational study of biomarker differences and does not test any treatment or prevention for Alzheimer's disease.
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The current conceptualization of Alzheimer disease (AD) is driven by the amyloid hypothesis, in which a deterministic chain of events leads from amyloid deposition and then tau deposition to neurodegeneration and progressive cognitive impairment.
Why it matters
This paper proposes a revised 'probabilistic' model of Alzheimer's disease in which the amyloid cascade plays a smaller role in sporadic forms than in autosomal dominant forms, with random factors playing a larger role. The authors say this model could help guide research and the development of prevention and treatment strategies.
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CSF synaptic biomarkers increase in the early preclinical stages of the Alzheimer continuum even when a low burden of Aβ pathology is present, and they differ in their association with age, sex, APOE ε4 , and markers of neurodegeneration.
Why it matters
In middle-aged cognitively unimpaired participants, several CSF synaptic biomarkers increased with age and with higher amyloid load, even in people at the earliest preclinical stage. These are marker findings and do not show that any treatment, cure, or prevention works.
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These results indicate that trans-resveratrol has potential neuroprotective roles in the treatment of moderate to mild AD and that its mechanism may involve a reduction in the accumulation and toxicity of Aβ in the brain of patients, thereby reducing neuroinflammation.
Why it matters
In 30 patients with mild to moderate Alzheimer's disease, changes in blood and CSF Aβ40 with trans-resveratrol were not statistically significant, while the placebo group showed a significant decrease in Aβ40. This small study does not show that trans-resveratrol treats, cures, or prevents Alzheimer's disease.
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These findings suggest that DPP-4i use is associated with low amyloid burden and favorable long-term cognitive outcome in diabetic patients with ADCI.
Why it matters
In a review of 282 patients with diabetes and Alzheimer-related cognitive impairment, those taking DPP-4 inhibitors had lower amyloid burden on PET scans and a slower decline in MMSE scores than those not taking them. This is an observational association and does not prove that DPP-4 inhibitors treat or prevent Alzheimer's disease.
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Co-pathologies play an important role in the expression of the Alzheimer's disease clinical phenotype and may influence treatment efficacy.
Why it matters
This autopsy study compared the frequency of common neuropathological diagnoses in 96 patients with early-onset Alzheimer's disease and 48 with late-onset disease. It describes co-pathology and does not test any treatment.
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Three women (aged 61, 72, and 73 years) consecutively enrolled in the trial successfully completed repeated focused ultrasound-induced BBB opening of the hippocampus and entorhinal cortex.
Why it matters
In this small early trial, three women with early Alzheimer's disease safely underwent repeated focused ultrasound to open the blood-brain barrier in memory-related brain regions. The study only reports that the procedure was completed successfully and does not show whether it improves memory or changes the disease course.
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There were detectable WMH, enlarged PVS, infarcts, and microbleeds as early as the 5th decade of life.
Why it matters
In adults with Down syndrome, this cross-sectional study found signs of cerebrovascular disease on MRI as early as the fifth decade of life. It describes when these brain changes appear and how they relate to amyloid and cognitive status, but it does not test a treatment or prevention.
From across this topic
10 of the 5,374 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.
- Multi Layered Omics Approaches Reveal Glia Specific Alterations in Alzheimer's Disease: A Systematic Review and Future Prospects
- The role of magnetic resonance imaging in the diagnosis of Alzheimer disease in adults with Down syndrome
- Candidate Gene for the Chromosome 1 Familial Alzheimer's Disease Locus
- Astrocyte reactivity influences amyloid-β effects on tau pathology in preclinical Alzheimer's disease
- Cerebral infarctions and the likelihood of dementia from Alzheimer disease pathology
- β-Amyloid in Cerebrospinal Fluid: How to Keep It Floating (Not Sticking) by Standardization of Preanalytic Processes and Collection Tubes
- Type 2 Diabetes Interacts With Alzheimer Disease Risk Factors to Predict Functional Decline
- Seizures in Cerebral Amyloid Angiopathy
- Why do so many drugs for Alzheimer's disease fail in development? Time for new methods and new practices?
- APOE, vascular pathology, and the AD brain