Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Highest usefulness score first. Studies without a score come last.
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Disease-modifying therapies for Alzheimer's disease (AD) are likely to be most beneficial when initiated in the presymptomatic phase.
Why it matters
In autosomal dominant Alzheimer's disease, cerebrospinal fluid and plasma neurofilament light chain trajectories were similar at presymptomatic stages and discriminated mutation carriers from non-carrier controls 10-20 years before estimated symptom onset, but after symptom onset the rate of change in cerebrospinal fluid continued to increase while the rate in plasma leveled off. Both plasma and cerebrospinal fluid changes were associated with grey-matter atrophy but not with Aβ-PET changes, supporting neurofilament light chain in both fluids as an early marker of neurodegeneration, though this concerns monitoring rather than treatment, cure, or prevention.
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Mean annual costs for individuals with clinically diagnosed AD were SEK 99,906, SEK 290,972, SEK 479,524, and SEK 795,617 in mild cognitive impairment (MCI), mild, moderate, and severe AD.
Why it matters
This registry-based cohort study found mean annual costs for individuals with clinically diagnosed Alzheimer's disease of SEK 99,906 in mild cognitive impairment, SEK 290,972 in mild, SEK 479,524 in moderate, and SEK 795,617 in severe disease. It describes costs by severity and does not test any treatment, cure, or prevention.
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63/100
It remains unclear which risk factors accelerate brain atrophy along with a progression from normal cognition to mild cognitive impairment (MCI).
Why it matters
Using long-term data from middle-aged and older adults, this cohort study examined which risk factors are linked to faster brain atrophy and progression from normal cognition to mild cognitive impairment. It identifies associations over time but does not show that changing these factors prevents progression.
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A summary measure of γ-secretase activity (γ-secretase composite [GSC]) was calculated for each variant and compared with clinical history-derived AAO using correlation analyses.
Why it matters
In people with inherited (autosomal dominant) Alzheimer's caused by PSEN1 variants, lower activity of γ-secretase, an enzyme involved in making amyloid β, was associated with earlier age at symptom onset. The authors suggest this partly explains clinical differences between people with the inherited form, support targeting γ-secretase as a treatment approach, and propose cell-based models to help predict when symptoms will start.
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We constructed models for MCI and mild dementia that predict MMSE over time.
Why it matters
This study built models using data from 961 amyloid-positive participants with mild cognitive impairment or mild dementia to predict cognitive decline over time. It is a prediction modeling study and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Across the cohort of 212 individuals with SCD+ (M(Age) = 69.17 years, F 42.45%), 258 individuals with MCI (M(Age) = 72.93, F 43.80%), and 195 individuals with dementia (M(Age) = 74.07, F 48.72%), no main effect of education (ß = 0.52, 95% CI -0.30 to 1.58), but a significant education-by-group interaction on CL values, was found ( p = 0.024) using linear regression modeling.
Why it matters
Across people with subjective cognitive decline, mild cognitive impairment, and dementia, years of education showed no overall link to amyloid burden, though there was an interaction with group. The study only examines an association with amyloid and does not test any treatment, cure, or prevention.
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Differential eligibility may contribute to underrepresentation of some minoritized racial and ethnic groups in early AD trials.
Why it matters
This analysis of screening data from four trials found that Hispanic, Black, and Asian participants had higher probabilities of being ineligible for amyloid biomarker criteria than non-Hispanic White participants. This concerns fairness in who can join Alzheimer's trials, not treating, curing, or preventing the disease.
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Mild cognitive impairment (MCI) is often considered an early stage of dementia, with estimated rates of progression to dementia up to 80-90% after approximately 6 years from the initial diagnosis.
Why it matters
Working out whether mild memory problems are caused by Alzheimer's usually needs spinal-fluid tests or brain scans, which the authors note only "a limited percentage of the population" can access. This review of 29 studies found that researchers increasingly combine blood, spinal-fluid or saliva markers with brain imaging, memory tests and genetics in machine-learning models, an approach the authors say "has shown promise" but which is not yet a proven diagnostic test. They call for cheaper, long-term data from culturally diverse populations and for "white-box" (interpretable) models.
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Pericyte damage, reflected by CSF PDGFRβ, may be involved in age-related BBB disruption together with neuroinflammation, but is not related to Alzheimer-related pathologic changes.
Why it matters
In 771 participants, higher cerebrospinal fluid PDGFRβ was related to higher age and was studied in relation to blood-brain barrier damage, neuroinflammation and Alzheimer pathologic changes. This is an observational biomarker study and does not report a treatment, cure or prevention.
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The study included 722 911 hospitalization episodes, of which 66 676 were related to patients with ADRD (mean [SD] age, 83.4 [8.6] years; 42 439 [63.6%] female) and 656 235 were related to patients without ADRD (mean [SD] age, 66.0 [15.4] years; 351 246 [53.5%] female).
Why it matters
This cohort study found that patients with Alzheimer disease and related dementias had higher 30-day readmission rates and higher readmission and episode costs than patients without these conditions. It suggests hospitals may need to be better equipped to care for these patients, but it does not test a dementia treatment or cure.
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Alzheimer's Disease (AD) represents the most common type of dementia and is becoming a steadily increasing challenge for health systems globally.
Why it matters
This meta-analysis found that inflammatory bowel disease (odds ratio 1.91) and rheumatoid arthritis (1.90) were linked to a higher risk of dementia, as was high C-reactive protein (CRP), an inflammation marker, in midlife (1.62). The authors say people with chronic inflammation showed a higher dementia risk and that better control of inflammation in people with chronic inflammatory or autoimmune conditions should be a priority. Tracking CRP over time might help estimate a person's risk.
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ATN (β-amyloid [Aβ], tau, neurodegeneration) system categorizes individuals based on their core Alzheimer disease (AD) biomarkers.
Why it matters
This cross-sectional study applied the ATN biomarker system in a real-life memory clinic and estimated who might be eligible for anti-amyloid treatment once such disease-modifying treatments become widely available. It does not report whether any treatment actually worked, only how eligibility could be assessed.
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This study suggests that early tau deposition may follow multiple trajectories during preclinical AD and may involve several cortical regions.
Why it matters
In preclinical Alzheimer disease, early tau deposition appeared to follow multiple trajectories and may involve several cortical regions, with increased regional tau linked to reduced hippocampal volume and medial temporal thickness. This is an observational imaging study and does not test any treatment, cure, or prevention.
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Alzheimer's disease (AD) is a devastating neurodegenerative disorder with no cure, and available treatments are only able to postpone the progression of the disease.
Why it matters
This systematic review and meta-analysis summarized existing prediction models for conversion from mild cognitive impairment to Alzheimer's disease and identified the most common factors used in those models. The authors state that such models are needed to allow early treatment of patients with MCI before they develop Alzheimer's disease.
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63/100
Further analyses to determine clinical utility are warranted.
Why it matters
Using a data-driven model on amyloid PET from several cohorts, this study identified three subtypes of amyloid accumulation, named frontal, parietal, and occipital, with different proportions of APOE ε4 carriers and dementia. This describes patterns of amyloid spread and does not test any treatment, cure, or prevention.
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Strikingly gene-expression, network-based analysis and cell type deconvolution approaches revealed a consistent immune signature in the brain and blood of female AD patients that was absent in males.
Why it matters
This meta-analysis found a consistent immune signature in the brain and blood of female Alzheimer's disease patients that was absent in males, and classification accuracy improved when results were split by sex. These findings are about immune differences and biomarkers and do not test any treatment, cure or prevention.
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Amyloid accumulation was evaluated in 236 individuals who underwent >1 amyloid PET scan.
Why it matters
In cognitively normal people with brain amyloidosis, the estimated age at which amyloid reached a low tipping point predicted the age at symptom onset of Alzheimer dementia. This is a prediction model and does not show that any treatment, cure, or prevention works.
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Alzheimer's disease is the primary cause of dementia worldwide, with an increasing morbidity burden that may outstrip diagnosis and management capacity as the population ages.
Why it matters
This study developed a deep learning framework that uses MRI, age, gender, and Mini-Mental State Examination score to classify Alzheimer's disease and visualize individual risk. It is a diagnostic tool validated across several datasets, not a treatment, cure, or prevention of the disease.
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We enrolled a cohort of 1070 PSEN1 E280A mutation carriers and 1074 non-carriers with baseline assessments; of these participants, longitudinal measures (with a mean follow-up of 6 years) were available for 242 mutation carriers and 262 non-carriers.
Why it matters
In the Colombian presenilin 1 E280A kindred, plasma NfL increased with age in both carriers and non-carriers, and the study characterized when concentrations begin to differ. The authors support plasma NfL as a biomarker for detection and tracking and for evaluating therapies, not as a treatment, cure or prevention.
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Intracranial atherosclerotic disease (ICAD) is an important cause of stroke and has also been recently identified as an important risk factor for all-cause dementia, but the mechanism of its association with cognitive performance is not fully understood.
Why it matters
This study tested whether intracranial atherosclerotic disease, a narrowing of brain arteries, is associated with amyloid-beta buildup in the brain. If confirmed, this could suggest that vascular disease contributes to Alzheimer's-related brain changes, though this was a cross-sectional analysis.
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Researchers quantified the phosphorylation state at multiple sites of the tau protein in cerebrospinal fluid markers across four decades of disease progression in dominantly inherited Alzheimer's disease.
Why it matters
Reports a signature of soluble phosphorylated tau that links tau, amyloid and the stages of dominantly inherited Alzheimer's disease.
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Study objectives To determine the effect of self-reported clinical diagnosis of obstructive sleep apnea (OSA) on longitudinal changes in brain amyloid PET and CSF biomarkers (Aβ42, T-tau, and P-tau) in cognitively normal (NL), mild cognitive impairment (MCI), and Alzheimer's disease (AD) elderly.
Why it matters
In cognitively normal and mild cognitive impairment participants, those with self-reported obstructive sleep apnea showed faster increases in brain amyloid and tau biomarker changes over about 2.5 years, while no significant differences were seen in the Alzheimer's disease group. This is an observational longitudinal study and does not show that treating sleep apnea prevents or treats Alzheimer's disease.
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The degree to which Alzheimer's versus other neuropathologies contribute to the risk of Alzheimer's dementia is unknown.
Why it matters
This study examined the risk of Alzheimer's dementia attributable to pathologic Alzheimer's disease and eight other neuropathologies in 1,161 participants from two clinical-pathological studies of aging. It quantifies how much dementia risk is linked to different brain pathologies and does not report a treatment, cure, or prevention.
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63/100
The ApoE ε4 allele is the most significant genetic risk factor for late-onset Alzheimer disease.
Why it matters
In African American and Puerto Rican individuals, APOE epsilon4 alleles on an African ancestral background conferred lower Alzheimer disease risk than those on a European ancestral background. This helps explain population differences in APOE epsilon4 risk and may inform population-specific risk prediction, but it does not provide a treatment or cure.
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63/100
Median (interquartile range) CRP levels increased with mean (SD) age (43.3 [9.6] years, 0.95 mg/L [0.40-2.35 mg/L] vs 59.1 [9.6] years, 2.04 mg/L [0.93-4.75 mg/L] vs 61.6 [9.5] years, 2.21 mg/L [1.05-5.12 mg/L]; P Conclusions and relevance In this study, peripheral chronic low-grade inflammation in participants with ApoE4 was associated with shortened latency for onset of AD.
Why it matters
This cohort study examined whether chronic low-grade inflammation, measured by repeated C-reactive protein levels, interacts with APOE genotype to affect Alzheimer disease risk. It reports an association but does not test any treatment, cure, or prevention.
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.
- Positron Emission Tomography Imaging With [18F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes
- Association of higher levels of high-density lipoprotein cholesterol in elderly individuals and lower risk of late-onset Alzheimer disease
- Predictors of Antiamyloid Medication Utilization and Adherence Among People With Alzheimer Disease and Mild Cognitive Impairment
- Soluble pool of A? amyloid as a determinant of severity of neurodegeneration in Alzheimer's disease
- The Effect of APOE ε4 on Alzheimer's Disease Fluid Biomarkers: A Cross-Sectional Study Based on the COAST
- Small molecule therapeutics for tauopathy in Alzheimer's disease: Walking on the path of most resistance
- APOE Genotype and Alzheimer Disease Risk Across Age, Sex, and Population Ancestry
- Diversity and disparity in dementia: the impact of ethnoracial differences in Alzheimer disease
- Binding sites of amyloid beta-peptide in cell plasma membrane and implications for Alzheimer's disease
- The pathology of the substantia nigra in Alzheimer disease with extrapyramidal signs