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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In this study involving Chinese participants during the 20 years preceding clinical diagnosis of sporadic Alzheimer's disease, we observed the time courses of CSF biomarkers, the times before diagnosis at which they diverged from the biomarkers from a matched group of participants who remained cognitively normal, and the temporal order in which the biomarkers became abnormal.
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Higher eGFR was associated with increased levels of plasma p-tau217, p-tau181, Tau212-221, and Tau181-190 in individuals with cognitive impairment (cohort 1: R range, -0.24 to -0.59; P Conclusions and relevance In this study, CKD was associated with increased plasma levels of soluble tau, but for p-tau217 the associations were considerably lower than the association with Aβ positivity.
Why it matters
Chronic kidney disease was linked to higher plasma p-tau217 and p-tau181, and using ratios of phosphorylated to unphosphorylated tau reduced this interference. This is about improving the accuracy of Alzheimer's blood tests in people with kidney disease, not about treating, curing, or preventing the disease.
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The PubMed and Embase databases were searched for clinical trials of anti-Aβ immunotherapy published on or before January 12, 2022.
Why it matters
This meta-analysis assessed the incidence of amyloid-related imaging abnormalities (ARIA) in clinical trials of anti-β-amyloid immunotherapy and compared incidence among different agents and clinical characteristics. It focuses on a side effect of treatment rather than on whether the treatment cures or prevents Alzheimer's disease.
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69/100
For early detection of Alzheimer's disease, it is important to find biomarkers with predictive value for disease progression and clinical manifestations, such as cognitive decline.
Why it matters
This study compared cerebrospinal fluid and imaging markers in 282 patients to see which best predicted cognitive decline. It found that tau PET best predicted decline, and that while amyloid results were similar using fluid or imaging, results for tau and neurodegeneration were not interchangeable.
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In this single-center observational study, we included all individuals who visited the Alzheimer Center Amsterdam and had a clinical diagnosis of subjective cognitive decline (SCD), mild cognitive impairment (MCI), or probable AD dementia and were A+.
Why it matters
This single-centre observational study looked at how neuropsychiatric symptoms relate to cognitive functioning in people who were β-amyloid-positive across the Alzheimer's disease clinical spectrum. It describes associations over time and does not test any treatment, cure or prevention.
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Advances in molecular positron emission tomography (PET) have enabled anatomic tracking of brain pathology in longitudinal studies of normal aging and dementia, including assessment of the central model of Alzheimer's disease (AD) pathogenesis, according to which TAU pathology begins focally but expands catastrophically under the influence of amyloid-β (Aβ) pathology to mediate neurodegeneration and cognitive decline.
Why it matters
In tau PET scans of 443 adults, tau first appeared near the rhinal sulcus in clinically normal people. In 104 people followed for 2 years, it spread first to nearby temporal-lobe cortex and then beyond the temporal lobe. Faster spread was associated with higher baseline amyloid and medial temporal tau. The study offers a way to track early tau changes in natural-history studies and prevention trials, but it tested no treatment and does not show that amyloid causes the spread.
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PE-treated patients performed significantly better than placebo for the co-primary endpoints: change from baseline of Alzheimer's Disease Cooperative Study-Activities of Daily Living (ADCS-ADL; P = .03; 52% less decline) with a trend for Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog; P = .06; 66% less decline) scores at month 14.
Why it matters
In this phase 2b/3 trial, 347 patients with mild-to-moderate Alzheimer's disease were randomized to plasma exchange with albumin replacement or placebo. Treated patients showed significantly better scores on one co-primary endpoint with a trend on the other, but this does not establish that plasma exchange cures or prevents Alzheimer's disease.
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This study's findings suggest that PET imaging with [18F]flortaucipir could be used to identify the density and distribution of AD-type tau pathology and the presence of high levels of AD neuropathological change, supporting a neuropathological diagnosis of AD.
Why it matters
This study found that flortaucipir PET imaging could identify the density and distribution of Alzheimer's-type tau pathology and support a neuropathological diagnosis of Alzheimer's disease. It is a diagnostic imaging study and does not report a treatment, cure or prevention.
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Across the whole-sample, the single-modality models indicated significant correlations between the rate of cognitive decline and the first component of each imaging modality.
Why it matters
In this longitudinal imaging study, temporo-parietal tau pathology and anterior temporal neuroinflammation predicted cognitive decline in patients with symptomatic Alzheimer's disease pathology. The authors say the findings support the strategy of targeting tau and neuroinflammation in disease-modifying therapy against Alzheimer's disease.
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Nine studies were eligible for inclusion.
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Increasing evidence suggests an important role of liver function in the pathophysiology of Alzheimer disease (AD).
Why it matters
This cohort study examined whether blood markers of liver function are associated with cognitive dysfunction and with amyloid, tau, and neurodegeneration biomarkers for Alzheimer disease. It reports associations only and does not show that any liver-related treatment, cure, or prevention works.
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The mean (SD) age was 73.7 (6.0) years, and the mean (SD) follow-up time was 3.7 (1.2) years.
Why it matters
In 223 clinically normal older adults followed for about 3.7 years on average, a higher Framingham cardiovascular risk score was linked to faster cognitive decline. The authors report this effect was stronger in people with more amyloid in the brain ("synergistically with Aβ burden"). They suggest vascular risk "may complement imaging biomarkers" in spotting who may decline. This was an observational study and did not test whether treating vascular risk changes the outcome.
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This multicenter randomized clinical trial demonstrated the feasibility of sham-surgery-controlled stereotactic gene delivery studies in patients with AD.
Why it matters
In this phase 2 trial, AAV2-NGF did not show a significant difference from sham surgery on the primary cognitive outcome measure. The trial demonstrated the feasibility of sham-surgery-controlled stereotactic gene delivery, but not clinical benefit.
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We systematically searched PubMed for eligible studies reporting data on CSF biomarkers reflecting amyloid precursor protein metabolism (Aβ42, Aβ40), neurodegeneration (t-tau), and tangle pathology (p-tau) in symptomatic sporadic CAA cohorts vs controls and patients with Alzheimer disease (AD).
Why it matters
This meta-analysis assessed which core cerebrospinal fluid biomarkers are most altered in sporadic cerebral amyloid angiopathy compared with controls and patients with Alzheimer disease. It concerns diagnosis and biomarker profiles, not treating, curing or preventing Alzheimer disease.
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We aimed to investigate whether hippocampal TDP-43 is associated with increased rates of hippocampal atrophy.
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PurposeTelephone disclosure of genetic test results can improve access to services.
Why it matters
In this trial of 257 asymptomatic adults, disclosing Alzheimer's disease genetic risk by telephone was generally safe and occurred sooner than in-person disclosure, with anxiety and depression scores below clinical concern. It addresses how risk information is delivered and does not provide a treatment, cure, or prevention.
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Epidemiological studies have identified a robust association between type II diabetes mellitus and Alzheimer disease (AD), and neurobiological studies have suggested the presence of central nervous system insulin resistance in individuals with AD.
Why it matters
In a small pilot study of 20 people with mild cognitive impairment or mild Alzheimer's dementia, metformin was safe and associated with improved executive functioning, with trends toward improvement in learning, memory, and attention. No significant change in cerebral blood flow was observed, and the authors say further study is needed, so this does not establish metformin as a treatment.
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In this community-based cohort without dementia, florbetapir uptake is associated with older age and APOE genotype.
Why it matters
This study found that in a community-based cohort without dementia, elevated brain amyloid was associated with older age and APOE ε4 genotype. It also found that black race was associated with higher amyloid uptake, after adjusting for demographics, vascular risk factors, cognitive status, white matter hyperintensity volume, and APOE genotype.
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Each level increase in the severity of atherosclerosis or arteriolosclerosis was associated with significantly higher odds of Alzheimer's disease dementia (odds ratio [OR] for atherosclerosis 1·33, 95% CI 1·11-1·58; OR for arteriolosclerosis 1·20, 1·04-1·40).
Why it matters
In this cross-sectional study of elderly people, each step up in the severity of atherosclerosis or arteriolosclerosis in brain vessels went with higher odds of Alzheimer's disease dementia (odds ratios 1·33 and 1·20), and with lower scores in most areas of thinking, though not every one: atherosclerosis showed no clear link to working memory. Because both were measured at one point in time, the study shows a link, not that vessel disease causes dementia, and it tested no treatment.
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Among the 1430 cognitively normal participants included, the mean (SD) age was 79.5 (5.3) years, 49.4% were men, the mean duration of education was 14.3 years, and 25.4% were APOE ε4 carriers.
Why it matters
In this longitudinal study, decreasing ability to identify smells was associated with an increased risk of amnestic mild cognitive impairment. This suggests that a smell identification test may help identify people at higher risk, though it does not show that treating smell loss would prevent or delay dementia.
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These findings challenge current management practices of Alzheimer's patients.
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11 studies were identified, including 380 patients with AD, 68 with MCI and 293 healthy controls (HC).
Why it matters
This meta-analysis of 11 studies found that the nerve fiber layer of the retina is thinner in people with mild cognitive impairment and even more so in people with Alzheimer's disease compared with healthy controls. The authors suggest this could help monitor progression and assess treatments, but the analysis does not test any treatment itself.
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The Alzheimer's Disease Neuroimaging Initiative (ADNI) is an ongoing, longitudinal, multicenter study designed to develop clinical, imaging, genetic, and biochemical biomarkers for the early detection and tracking of Alzheimer's disease (AD).
Why it matters
This article reviews papers from the Alzheimer's Disease Neuroimaging Initiative, a long-running study that collects clinical, imaging, genetic and biochemical markers to detect and track Alzheimer's disease early. Its main contribution is to research tools and biomarkers, not a treatment or cure.
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¹⁸F-FDFG uptake by brain tissue as measured by positron emission tomography (PET) is a well-established method for assessment of brain function in people with dementia.
Why it matters
This review assessed how accurately ¹⁸F-FDG PET detects which people with mild cognitive impairment will later convert to Alzheimer's disease dementia or other dementias. It is about diagnosis, not treatment, cure or prevention.
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Whether novel risk variants of Alzheimer's disease (AD) identified through genome-wide association studies also influence magnetic resonance imaging-based intermediate phenotypes of AD in the general population is unclear.
Why it matters
In this meta-analysis, a genetic risk score for Alzheimer disease was associated with smaller hippocampal volume, though only the association including APOE remained significant after correcting for multiple tests. It suggests risk genes may affect brain structure in people without dementia, but shows no treatment 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.
- ADAMTS4 is involved in the production of the Alzheimer disease amyloid biomarker APP669-711
- Dietary intake of antioxidants and risk of Alzheimer disease
- A randomized, double-blind, placebo-controlled trial of resveratrol for Alzheimer disease
- Relationships of Dietary Patterns, Foods, and Micro- and Macronutrients with Alzheimer's Disease and Late-Life Cognitive Disorders: A Systematic Review
- Astrocytes: conductors of the Alzheimer disease neuroinflammatory symphony
- A novel tau-based rhesus monkey model of Alzheimer's pathogenesis
- Phases of Aβ-deposition in the human brain and its relevance for the development of AD
- Combined CSF tau, p-tau181 and amyloid-beta 38/40/42 for diagnosing Alzheimer's disease
- Evidence of oxidative stress in Alzheimer's disease brain and antioxidant therapy: lights and shadows
- Decrease of evoked delta, theta and alpha coherences in Alzheimer patients during a visual oddball paradigm