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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Our results demonstrate that unsupervised digital memory assessments might be used for diagnosis and prognosis in Alzheimer's disease, potentially in combination with plasma biomarkers.
Why it matters
Remote memory tests done by people at home on mobile devices were usable, valid, and reliable, and were linked to tau PET scans and brain MRI measures, and memory performance predicted future cognitive decline, especially when combined with a blood marker called plasma p-tau217. This study is about improving diagnosis and prognosis, not about treating, curing or preventing Alzheimer's disease.
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Ten papers were identified from 7 studies.
Why it matters
This review of 10 papers found little evidence linking amyloid PET disclosure to depression, but people with mild cognitive impairment and their caregivers who had elevated amyloid had increased risk of distress or anxiety. It found mixed evidence on psychosocial and behavioral outcomes and no studies measuring behavioral outcomes.
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54/100
Alzheimer's Disease (AD) contributes to most cases of dementia.
Why it matters
This review notes that amyloid-targeting therapies have been the focus of drug development and that two such drugs received accelerated FDA approval, but their efficacy or long-term safety remains uncertain. It reports no established cure or prevention.
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Alzheimer's disease (AD), the most common cause of dementia, results in a sustained decline in cognition.
Why it matters
This review discusses the gut microbiome as a possible upstream modulator of amyloid, tau and neuroinflammation in Alzheimer's disease, while noting there are currently few effective disease-modifying therapies. It offers no confirmed treatment, cure or prevention.
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CSF biomarkers β-amyloid 1-42 (Aβ 42 ), phosphorylated tau 181 (p-tau 181 ), total tau (t-tau), and neurogranin (Ng) can diagnose Alzheimer disease (AD) in life.
Why it matters
This study checked whether having both Alzheimer's and alpha-synuclein pathology at autopsy changes CSF levels of amyloid, tau and neurogranin. It is about whether these biomarkers remain accurate when another brain disease is also present, not about treatment.
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Alzheimer's disease (AD) is the most common cause of dementia worldwide, and its prevalence is rapidly increasing due to extended lifespans.
Why it matters
This review describes how the APOE gene, especially the ε4 allele, increases Alzheimer's disease risk while the ε2 allele is protective, and how apoE relates to amyloid-beta. It discusses challenges in designing apoE-targeted therapeutic strategies but reports no proven treatment or cure.
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54/100
Early diagnosis of Alzheimer's disease plays a pivotal role in patient care and clinical trials.
Why it matters
This study developed a deep learning model that uses structural MRI scans to distinguish mild Alzheimer's dementia from mild cognitive impairment and normal cognition. It is a diagnostic tool and does not treat, cure, or prevent the disease.
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Microglial activation distributes preferentially along highly connected brain regions, similar to tau pathology.
Why it matters
In 32 amyloid-positive early Alzheimer disease subjects and 18 amyloid-negative controls, microglial activation measured by TSPO-PET was distributed along functionally highly connected brain regions, and patients showed increased tracer uptake in some areas. This is an imaging study of microglial activation and brain connectivity, not a treatment, cure or prevention for Alzheimer's disease.
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Alzheimer's disease (AD) is a devastating neurodegenerative disorder characterized by gradual loss of memory and cognitive function, which constitutes a heavy burden on the healthcare system globally.
Why it matters
This review states that emerging evidence indicates endoplasmic reticulum stress contributes to the onset and development of Alzheimer's disease and that current therapeutics to interfere with the underlying disease process are still under development. It discusses possible therapeutic avenues but tests no treatment, cure, or prevention.
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Alzheimer's disease (AD) is the most frequently occurring type of dementia.
Why it matters
This UK Biobank study of 483,507 participants found a non-linear relationship between sleep duration and Alzheimer's disease incidence over an average 11.3 years of follow-up. It is an observational study, so it cannot show that changing sleep duration prevents Alzheimer's disease.
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Longitudinal patterns of clinical decline differ between LPA and PCA but are heterogeneous and related to different patterns of topographic spread.
Why it matters
In this case-control study of 28 patients with posterior cortical atrophy and 27 with logopenic progressive aphasia, the two atypical Alzheimer disease variants showed different patterns and rates of clinical decline linked to regional brain atrophy. This describes how these variants progress and does not test a treatment or cure.
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These results revealed a universal applicability of the "A/T/N" framework in a Chinese population and established an optimal diagnostic model consisting of cost-effective and non-invasive approaches for diagnosing AD.
Why it matters
A combination of plasma p-tau, APOE genotype, and MRI measures accurately predicted amyloid PET status, and fluid biomarkers helped discriminate Alzheimer's disease from other dementias. This is about improving diagnosis, not about treating, curing, or preventing the disease.
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These findings suggest that at current expected prices, neither aducanumab nor donanemab would be cost-effective for early AD in the US.
Why it matters
This analysis found that at current expected prices, neither aducanumab nor donanemab would be cost-effective for early Alzheimer's disease in the US. It addresses cost and value rather than whether the drugs work, and it does not support these treatments as cost-effective options.
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Amyloid-β (Aβ) pathology is one of the earliest detectable brain changes in Alzheimer's disease (AD) pathogenesis.
Why it matters
Amyloid PET scans are usually read by eye as simply "positive" or "negative", but this review argues that amyloid builds up continuously and that binary cut-offs alone do not capture it well. It reports that quantitative, tracer-independent measures can flag changes at the earliest stages of Alzheimer's, sharpen diagnostic confidence, and, according to large multi-centre studies it cites, predict rates of cognitive decline. It is a review about diagnosis and choosing who enters trials; it does not test any treatment.
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The Electrophysiology Professional Interest Area (EPIA) and Global Brain Consortium endorsed recommendations on candidate electroencephalography (EEG) measures for Alzheimer's disease (AD) clinical trials.
Why it matters
This expert panel recommends standardizing resting-state EEG recording and using certain brain wave measures to group patients and monitor disease progression and interventions in Alzheimer's disease trials. These are recommendations for measurement in trials, not evidence that any treatment works.
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The aim of this study was to provide an update on the role of the innate immune system and neuroinflammation in the pathogenesis of Alzheimer's disease, with an emphasis on microglial receptors CD33 and TREM2.
Why it matters
This review reports that many Alzheimer's risk genes relate to the innate immune system and microglia, including CD33 and TREM2, and that disease-associated microglia show TREM2-dependent changes. It describes risk biology and does not report a treatment, cure or prevention.
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Despite the increasing incidence and high morbidity associated with dementia, a simple, non-invasive, and inexpensive method of screening for dementia is yet to be discovered.
Why it matters
A deep learning system distinguished faces of patients with mild dementia from those without dementia with high accuracy in this sample. It is a screening study only and reports no treatment, cure, or prevention.
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Recent studies suggest that plasma phosphorylated tau181 (p-tau181) is a highly specific biomarker for Alzheimer's disease (AD)-related tau pathology.
Why it matters
This study examined whether a genetic risk score for Alzheimer's disease is associated with plasma phosphorylated tau181, a biomarker proposed for diagnosis and prognosis. It is a biomarker association study, so it does not test any treatment, cure, or prevention.
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Alzheimer's disease (AD), the most common form of dementia, is recognized as a heterogeneous disease with diverse pathophysiologic mechanisms.
Why it matters
By analyzing 1543 transcriptomes from two Alzheimer's disease cohorts, this study identified three molecular subtypes of the disease involving different dysregulated pathways. It describes disease heterogeneity and does not test or establish any treatment, cure or prevention.
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Late-onset Alzheimer's disease (LOAD) is the most common form of dementia worldwide.
Why it matters
This work presents a systems biology approach to compare mouse models of late-onset Alzheimer's disease with human brain gene expression modules associated with the disease. It is a research tool for aligning animal models with human molecular signatures, not a treatment, cure or prevention.
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To provide better prevention and treatment, we need to understand the environmental and genetic risks of Alzheimer's disease (AD).
Why it matters
This analysis stresses that Alzheimer's disease has often been confounded with dementia in studies, and that genetic findings have been overinterpreted when it comes to mechanisms and drug targets. It concludes that the lack of mechanistic understanding of genetic variation is the major bottleneck in finding new drug targets, and does not report any treatment result.
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Low serum albumin may increase the risk of AD dementia by elevating amyloid accumulation.
Why it matters
In older adults without dementia, lower serum albumin was associated with higher amyloid deposition in the brain, but albumin levels were not related to brain metabolism, cortical thickness, or white matter hyperintensities. This suggests low albumin may relate to amyloid buildup, but the study does not show that raising albumin prevents or treats Alzheimer's disease.
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ApoE isoforms influence mitochondrial structure and function, which likely leads to alteration in oxidative stress, synapses, and cognitive function.
Why it matters
In postmortem brain tissue from 46 cases, ApoE-ε4 carriers showed impaired mitochondrial structure and function, oxidative stress, and synaptic damage compared to noncarriers. These mitochondrial and synaptic proteins were strongly associated with cognitive performance, but the study is observational and does not test any intervention.
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Our proof-of-concept study is the first to show that microstructural and macrostructural changes can reflect underlying neuroinflammatory mechanisms in early stages of Alzheimer disease (AD).
Why it matters
This small study in families with autosomal-dominant Alzheimer disease used PET and MRI to look at astrocytosis and cortical microstructure in mutation carriers. It is early research into brain changes before and after symptoms, not a treatment or cure.
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Fluid and imaging biomarkers of Alzheimer disease (AD) are often used interchangeably, but some biomarkers may reveal earlier stages of disease.
Why it matters
This study characterized people with tau abnormality shown by cerebrospinal fluid assay or PET, since these biomarkers may reveal different stages of disease. It is about diagnosis and does not test any treatment or cure.
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.
- An Update on Blood-Based Markers of Alzheimer's Disease Using the SiMoA Platform
- Clinical trial of an inhibitor of RAGE-Aβ interactions in Alzheimer disease
- Soluble TREM2 changes during the clinical course of Alzheimer's disease: A meta-analysis
- Sex-Specific Cross Tissue Meta-Analysis Identifies Immune Dysregulation in Women With Alzheimer's Disease
- Stress as risk factor for Alzheimer's disease
- Down syndrome, Alzheimer's disease and seizures
- Inflammation context in Alzheimer's disease, a relationship intricate to define
- Reduced hippocampal functional connectivity in Alzheimer disease
- Processing of Alzheimer beta/A4 amyloid precursor protein: modulation by agents that regulate protein phosphorylation
- Very mild Alzheimer's disease: informant-based clinical, psychometric, and pathologic distinction from normal aging