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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52/100
In a general population sample, we determined incidence of dementia and of probable AD and will use these incident cases for study of precursors and natural history in this elderly cohort, which has been under close surveillance for over 40 years.
Why it matters
In the Framingham Study cohort followed for up to 10 years, dementia incidence doubled in each successive 5-year age group, from 7.0 per 1,000 at ages 65 to 69 to 118.0 per 1,000 at ages 85 to 89. Incidence of probable Alzheimer's disease also doubled with age, and neither rate leveled off with age or differed between men and women.
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The performances of 89 patients with dementia of the Alzheimer type (DAT) and 53 demographically matched elderly normal control subjects were compared on four verbal fluency measures (category, letter, first names, and supermarket fluency).
Why it matters
Category fluency discriminated best between patients with dementia of the Alzheimer type and normal controls, including in mildly impaired patients. This superiority is attributed to its dependence on semantic knowledge, which deteriorates in the early stages of the disease.
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The relationship of microglia and astrocytes to deposits of beta-amyloid protein (BAP) was studied in Alzheimer's disease by immunohistochemistry.
Why it matters
Staining brain tissue from people with Alzheimer's disease, this study found beta-amyloid in forms ranging from "diffuse amorphous deposits to compact spherical masses", with the compact ones matching classic senile plaques. "Nearly all compact deposits" had reactive (HLA-DR-positive) microglia "embedded in their core", and electron microscopy showed these cells "in intimate contact with amyloid fibrils", whereas about half of diffuse deposits had none. It shows where cells sit at a single point in time, not whether microglia cause, clear or respond to plaques; it gives no case numbers, its stored text reports no astrocyte finding, and it tested no treatment.
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Brains of 49 patients who had died with Alzheimer's disease and 54 controls were examined.
Why it matters
In brains of 49 patients who died with Alzheimer's disease, the study found reduced cholinergic marker enzyme activity and reduced noradrenaline, gamma-aminobutyric acid and somatostatin, with older patients showing a relatively pure cholinergic deficit in temporal lobe and hippocampus. It is a post-mortem neurochemical description and does not report any treatment, cure or prevention.
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Of 822 individuals enrolled in the HEAD study, 681 participants spanning cognitively unimpaired to dementia were included.
Why it matters
This study developed a standardized visual reading framework for tau PET scans that identified more tau-positive people in early disease stages compared to the currently approved method. It is a diagnostic staging tool and does not test any treatment, cure, or prevention.
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The study included 197 patients in whom lecanemab infusions had been started (lecanemab group), as well as 173 patients in whom lecanemab had been ordered but not yet started, who were combined with 1139 research participants with cognitive impairment from the Knight ADRC cohort to form the untreated control group with cognitive impairment (n=1312).
Why it matters
In patients treated with lecanemab, 34 of 130 plasma biomarkers showed significant changes, with some shifting toward levels seen in amyloid-negative people without cognitive impairment. The study describes biomarker changes during treatment but does not report whether this translates into curing or preventing Alzheimer's disease.
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Alzheimer disease (AD) is the most common cause of dementia in the world and its prevalence is increasing and it has important public health consequences.
Why it matters
This systematic review looked at how accurately blood-based biomarkers can detect Alzheimer disease early, compared with costly and invasive PET and CSF methods. It is about improving diagnosis, not about treating, curing or preventing the disease.
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51/100
The final study sample comprised 8,797 participants (53.5% women, mean age at HUNT4 77.8 [SD 6.2]).
Why it matters
Midlife central and general adiposity were linked to higher late-life p-tau217 and higher risk of biomarker-verified AD dementia, while late-life adiposity showed the opposite pattern. The authors identify midlife central and general adiposity as modifiable risk factors for AD pathology and dementia.
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Cerebral amyloid angiopathy (CAA) is a cerebrovascular disorder characterized by the deposition of amyloid-β (Aβ) in the walls of leptomeningeal and cortical blood vessels that increases risk of intracerebral hemorrhages and progressive cognitive decline.
Why it matters
This study used a plasma protein panel to explore biomarkers of cerebral amyloid angiopathy, a condition present in more than 90% of people with Alzheimer's disease and a significant risk factor for ARIA with anti-amyloid treatments. The authors report that a multi-analyte panel combined with blood biomarkers for Alzheimer's pathology may be able to identify CAA, which could improve risk stratification and reduce symptomatic ARIA.
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The prominent prognostic role of carotid plaques in Aβ-negative MCI underscores the vascular contributions to non-amyloid cognitive decline and highlights the importance of evaluating both AD-related and vascular mechanisms in prodromal dementia.
Why it matters
In 300 people with MCI followed for 37 months, higher amyloid burden, smaller hippocampal volume, greater carotid plaque count, and lower MMSE scores independently estimated risk of progressing to Alzheimer's dementia. The study suggests carotid atherosclerosis provides additional prognostic value, particularly in amyloid-negative MCI, but it is a risk prediction study and not a treatment trial.
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= 0.028), but not with progression of BG-EPVS or WMHs at follow-up.
Why it matters
This community-based cohort study found that accelerated biological aging was associated with higher odds of cerebral small vessel disease progression, especially new lacunes and new microbleeds. It suggests biological age markers may help identify people at higher risk, but does not test any treatment or prevention.
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The study describes 4 males who developed dementia following confirmed or suspected c-hGH treatment in childhood (age at symptom onset between 47 and 60 years) with cognitive syndromes characterized by prominent language involvement.
Why it matters
This describes four men who developed dementia after receiving c-hGH treatment in childhood, with one showing clear Alzheimer's-type brain changes at autopsy. It suggests that in rare cases Alzheimer's disease can be acquired through medical treatment, but this is a small case series and does not apply to most people with Alzheimer's.
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Early and accurate detection of Alzheimer's disease (AD) is essential for timely intervention and development of disease-modifying treatments.
Why it matters
Using the German DELCODE cohort of people at early stages of memory decline, researchers compared GFAP, a marker of reactive astrocytes (support cells in the brain), measured in blood versus spinal fluid. GFAP rose across the Alzheimer's continuum, and blood GFAP outperformed spinal fluid GFAP in detecting amyloid and was linked to higher risk of clinical progression. The authors conclude blood GFAP is a sensitive, minimally invasive marker that may aid early diagnosis and prognosis.
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Microglia are implicated in the progression of Alzheimer's disease (AD) pathology from its earliest stages, suggesting that cerebrospinal fluid (CSF) microglia profiling across clinical AD stages can aid in treatment development and monitoring.
Why it matters
Analyzing cerebrospinal fluid from 834 people, this study identified 109 dysregulated microglia-related proteins and an 18-protein panel that differed between preclinical and dementia stages of Alzheimer's disease. This is biomarker research for staging and monitoring, not a treatment or prevention.
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In the ADMET2 biomarker subset (n = 44, MPH:21, age:75 years, MMSE:20.2), higher baseline TNF was associated with higher M6 NPI-A [B(SE)= 6.86 (1.71), p = .0003], and multivariable models found lower baseline TNF [B(SE)= 8.28(1.61), p < .001] and higher baseline S100B [B(SE)= -6.41(1.95), p = .002] were associated with lower M6 NPI-A. Exploratory analyses suggested that higher baseline NfL significantly interacted with treatment to predict lower M6 NPI-A [B(SE)= -8.36(4.21), p = .05], only when adjusting for cognition.
Why it matters
In a secondary analysis of 44 participants from a methylphenidate trial for apathy in dementia, baseline levels of inflammatory and neuronal injury markers (TNF, S100B, NfL, IL-6) were associated with apathy outcomes and with response to methylphenidate. These exploratory findings suggest biomarkers may one day help guide treatment of apathy, but they do not show any effect on curing or preventing Alzheimer's disease.
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51/100
As evidence supporting the robustness of blood-based biomarker (BBM) testing for Alzheimer disease (AD) continues to emerge, understanding the perceptions, drivers, and barriers to the adoption of these tests among primary care physicians (PCPs) in the United States is crucial for improving patient outcomes and advancing clinical management of AD.
Why it matters
This survey of U.S. primary care physicians examined practices and barriers around blood-based biomarker testing for early detection of Alzheimer's disease. It reports on diagnosis and adoption of testing, not on treating, curing, or preventing the disease.
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The DABNI cohort included 1,135 participants with a mean age of 42.82 years (SD = 11.56), 46.3% of whom are female.
Why it matters
This ten-year study of over 1,100 people with Down syndrome found that Alzheimer's progression is rare before age 40 but common after 50, with a long predictable phase before symptoms. The findings support using this population to study early Alzheimer's and to test interventions.
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Of the 250 participants, 121 (48.4%) were female and the mean age at follow-up was 76.06 (SD 0.48).
Why it matters
In 250 cognitively healthy older adults followed for 5 to 7 years, lower cerebrospinal fluid Aβ42/40 was associated with a steeper decline in processing speed, but no significant associations were found with changes in the other five cognitive domains or the composite score. The results suggest processing speed decline may appear before other cognitive changes in people with amyloid pathology, but this is an observational cohort study and does not test any treatment.
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White matter hyperintensity (WMH), indicative of cerebral small vessel disease, has emerged as a potential biomarker for cognitive decline in Alzheimer's disease (AD).
Why it matters
In people with mild cognitive impairment, higher white matter hyperintensity volume was linked to worse memory and language scores, though differences between cognitive groups were not statistically significant. The authors suggest white matter hyperintensity measurement may help identify early cognitive decline, but this is a cross-sectional study and does not test treatment.
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ADI groups differed by sex, ethnoracial background, and MMSE scores.
Why it matters
This study found that the accuracy of blood-based biomarkers for amyloid PET status did not differ across neighborhood disadvantage groups, supporting their use across socioeconomic settings. It is about diagnosis, not about treating, curing or preventing Alzheimer's disease.
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High correlations between plasma and serum were observed for most assays (ρ > 0.8), though plasma often yielded higher concentrations.
Why it matters
Serum p-tau217 correlated strongly with plasma p-tau217 across most assays and showed similar patterns across the Alzheimer's continuum, but absolute levels and cutoffs differed between the two. The authors conclude serum can be a viable alternative to plasma if matrix-specific validation is done.
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51/100
RBC DHA was associated with a positive (improved) global cognition (PACC) rate of change (estimate: 0.011; 95% CI: 0.001, 0.021; P = 0.024).
Why it matters
In individuals at risk of Alzheimer disease, higher red blood cell DHA was associated with improved global cognition rate of change and higher ALA with better visual processing, with no significant interactions for sex, APOE-ε4 carriership, or AD pathology. These are observational associations, and the authors say they add to observational evidence linking ω-3 fatty acids with brain health.
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Cognitive impairment and dementia, including Alzheimer's disease (AD), pose a global health crisis, necessitating non-invasive biomarkers for early detection.
Why it matters
This review describes retinal changes as possible non-invasive markers for early diagnosis and risk stratification in cognitive impairment and dementia. It states that translating these markers into practice faces hurdles such as inconsistent methods, confounding factors, and insufficient long-term validation, so no treatment or cure is offered.
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Advancing the understanding and management of Alzheimer's disease and related dementias requires integrating and analyzing diverse data modalities.
Why it matters
This perspective proposes an 'AI-first' approach to combining different kinds of data, such as imaging, wearable sensors and speech, for Alzheimer's disease and related dementias. It is a proposal about data standards and infrastructure, not a study of any treatment, prevention or cure.
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Our findings suggest that microglial and astrocyte reactivity, measured through fluid biomarkers, occur early and impact the amyloid cascade on the preclinical Alzheimer´s continuum.
Why it matters
In 211 cognitively unimpaired people, plasma GFAP and CSF sTREM2 were increased in preclinical Alzheimer's disease, and the findings suggest microglial and astrocyte reactivity occurs early and affects the amyloid cascade. This is about early biomarker changes, not about treating, curing or preventing the disease.
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.
- The Diagnosis of Mild Cognitive Impairment due to Alzheimer’s Disease: Recommendations from the National Institute on Aging-Alzheimer’s Association Workgroups on Diagnostic Guidelines for Alzheimer’s Disease
- Nonsteroidal antiinflammatory drugs and the risk of Alzheimer's disease
- Integrating plasma p-tau217 and digital cognitive assessments for early detection in Alzheimer's disease
- Amyloid probability in Alzheimer disease from plasma, cerebrospinal fluid, and amyloid imaging
- Association of Brain DNA methylation in SORL1, ABCA7, HLA-DRB5, SLC24A4, and BIN1 with pathological diagnosis of Alzheimer disease
- Pre-dementia clinical stages in presenilin 1 E280A familial early-onset Alzheimer's disease: a retrospective cohort study
- Real-world safety and implementation challenges of lecanemab therapy for Alzheimer's disease in South Korea: a single-center experience
- Evidence that the 42- and 40-amino acid forms of amyloid beta protein are generated from the beta-amyloid precursor protein by different protease activities
- Artificial intelligence in atrial fibrillation – Timely diagnosis, risk assessment and personalized management
- A randomized controlled trial of high-dose vitamin D2 followed by intranasal insulin in Alzheimer's disease