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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Overall, the study with the same protocol is going as expected with no serious AE or any major protocol deviation.
Why it matters
This is a protocol paper describing how an ongoing randomized trial of repetitive transcranial magnetic stimulation will be analyzed partway through, so it does not yet report whether the treatment works. Enrollment has been slowed by the COVID-19 pandemic, and no serious adverse events or major protocol deviations have occurred so far.
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Amyloidogenicity and vascular dysfunction are the key players in the pathogenesis of Alzheimer's disease (AD), involving dysregulated cellular interactions.
Why it matters
This review describes how the balance between neurons, astrocytes, microglia, oligodendrocytes and vascular cells sustains normal neuronal circuits, and how glial dyshomeostasis promotes the Alzheimer's-associated neurodegenerative cascade. It also notes that cerebrovascular diseases overlap neuropathologically with Alzheimer's disease, suggesting that vascular dysfunction is a key player in its pathogenesis.
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Alzheimer's disease (AD) has emerged as a key comorbidity of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2).
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Astrocyte reactivity is a hallmark of neuroinflammation that arises with Alzheimer's disease (AD) and nearly every other neurodegenerative condition.
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The gut microbiota (GM) represents a diverse and dynamic population of microorganisms and about 100 trillion symbiotic microbial cells that dwell in the gastrointestinal tract.
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43/100
Alzheimer's disease is a progressive, clinically heterogeneous, and particularly complex neurodegenerative disease characterized by a decline in cognition.
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43/100
The microbiota-gut-brain axis plays an important role in the development of neurodegenerative diseases.
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It accounts for a quarter of the elderly population and is associated with cognitive decline.
Why it matters
This imaging study compared brain functional impairment patterns in people with suspected non-Alzheimer disease pathophysiology (negative amyloid but abnormal tau) versus Alzheimer's disease. It is a brain-imaging comparison, so it does not show a treatment, cure or prevention.
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43/100
The white matter FC decreased in late MCI and AD dementia patients compared to CN participants, and this decrease was correlated with cognitive measures.
Why it matters
This study of 383 people found that functional connectivity in white matter decreased with cognitive decline in Alzheimer's disease, with specific regional deficits appearing in late mild cognitive impairment and Alzheimer's dementia, and these changes correlated with thinking test scores. It is about using brain imaging as a marker of decline, not about treating, curing or preventing the disease.
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Our comprehensive examination of the genetic evidence for the causal relationships between previously reported risk factors in AD using PRS and MR supports a causal role for education, blood pressure, cholesterol levels, smoking, and diabetes with the AD phenome.
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There is growing evidence that promising biomarkers of inflammation in Alzheimer´s disease (AD) and other neurodegenerative diseases correlate strongest to levels of tau or neurofilament, indicating an inflammatory response to neuronal damage or death.
Why it matters
This study measured ferritin, FABP-3 and neurogranin in CSF and looked at how they relate to established Alzheimer's and inflammation markers. It investigates possible biomarker links but does not test any treatment or show a way to prevent the disease.
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Twenty-three patients with mild cognitive impairment (MCI), 12 dementia of Alzheimer's type (DAT), and 14 normal controls were studied following the ADNI2 protocol.
Why it matters
This 60-month follow-up classified Argentine participants by amyloid, tau and neurodegeneration biomarkers and described how they progressed. It shows these biomarkers may help predict outcomes, but it does not test any treatment or cure.
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Of the 1,193 CI patients, 860 (72.1%) were amyloid-positive.
Why it matters
In 1,193 people with cognitive impairment, amyloid PET was positive in 86.8% of those with Alzheimer's disease and in only 5.6% of those with frontotemporal dementia, and the APOE ε4 allele was more frequent in amyloid-positive cases. This supports amyloid imaging for differential diagnosis, not for treating, curing or preventing Alzheimer's disease.
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Observational studies strongly supported the association of low levels of circulating 25-hydroxyvitamin D (25OHD) and cognitive impairment or dementia in aging populations.
Why it matters
This study used a genetic method called Mendelian randomization to test whether vitamin D levels directly affect the risk of Alzheimer's disease. The approach helps distinguish causation from mere association, which is important because randomized trials have not shown clear cognitive benefits from vitamin D supplementation.
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43/100
Machine learning models are promising alternatives for estimating the genetic risk of LOAD.
Why it matters
Machine learning models using genetic data predicted late-onset Alzheimer's disease with about 72% area under the ROC curve, which is not high enough to be a stand-alone diagnostic test. This work may help identify new genetic markers linked to the disease, but it does not provide a treatment, cure or prevention.
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Down syndrome (DS) is the main genetic cause of intellectual disability worldwide.
Why it matters
This review describes that overexpression of amyloid precursor protein in Down syndrome leads to beta-amyloid deposition resulting in Alzheimer's disease and often cerebral amyloid angiopathy, with people with Down syndrome developing Alzheimer's neuropathology at age 40. It highlights the need for large biomarker-characterized cohorts and does not report a treatment or cure.
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Human and animal studies suggest that inflammation occurring outside the central nervous system (systemic inflammation) may play a key role in promoting neurodegeneration, Alzheimer's disease pathology, and cognitive decline in older adults.
Why it matters
This review discusses how inflammation outside the brain may promote neurodegeneration and Alzheimer's pathology and cognitive decline in older adults. It does not report a specific treatment, cure, or prevention for Alzheimer's disease.
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43/100
A plethora of complex misfolded protein combinations have been found in Alzheimer disease (AD) brains besides the classical pathological hallmarks.
Why it matters
Red blood cells from people with early Alzheimer disease had lower levels of alpha-synuclein and its complexes with amyloid-beta and tau than healthy controls. This suggests a possible peripheral marker, but the study was small and did not show whether measuring it helps diagnosis or treatment.
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43/100
Alzheimer's disease (AD) is the most common cause of dementia in the elderly and the sixth leading cause of death in the United States.
Why it matters
This genetic analysis corroborated previously detected Alzheimer's disease loci and found 35 single-nucleotide polymorphisms outside the chromosome 19q13 region at a suggestive significance level, including possible sex-specific contributors. It is a genetic association analysis and does not test any treatment, cure, or prevention.
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Alzheimer's disease (AD) affects nearly 50 million people worldwide, and currently no disease-modifying treatment is available.
Why it matters
This review discusses CD33 and immune-inflammatory pathways as possible targets in Alzheimer's disease and notes that no disease-modifying treatment is currently available. It is a summary of biology and target ideas, not evidence that any treatment, cure, or prevention works.
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Blood glucose homeostasis is well maintained by coordinated control of various hormones including insulin and glucagon as well as cytokines under normal conditions.
Why it matters
This review reports that hyperglycemia is closely related to cognitive impairment and dementia, suggesting a possible cause-effect relationship, and speculates that glucotoxicity may damage brain cells and increase amyloid beta accumulation. It does not test any treatment or prevention for Alzheimer's disease.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the most common cause of dementia.
Why it matters
This review describes how SPECT and PET imaging can detect beta-amyloid deposits, tau protein accumulation, and other pathological processes in Alzheimer's disease. The findings are about using imaging as biomarkers for early diagnosis and prediction of progression, not about treating, curing, or preventing the disease.
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Alzheimer's disease (AD) is characterized by neuronal loss and astrocytosis in the cerebral cortex.
Why it matters
Using cell-type deconvolution across three transcriptomic studies, this work found that neuronal and astrocyte proportions differ between healthy and diseased brains and among Alzheimer's disease-associated genetic variants. These are descriptive cellular findings and do not demonstrate a treatment, cure or prevention.
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Generated MR images from florbetapir PET showed signal patterns that were visually similar to the real MR. The structural similarity index between real and generated MR was 0.91 ± 0.04.
Why it matters
This study used deep generative networks to create structural MR images from amyloid PET scans, allowing accurate amyloid quantification without a real MR. It is a technical imaging method and does not test any treatment, cure or prevention.
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43/100
Alzheimer's disease (AD) is a frequently observed, irreversible brain function disorder among elderly individuals.
Why it matters
This study used resting-state fMRI and permutation entropy to examine brain signal complexity in people with mild cognitive impairment and Alzheimer's disease compared with normal controls. It is an imaging study of brain function, not a treatment, cure or prevention study.
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.
- Plasma Exosomal miRNAs in Persons with and without Alzheimer Disease: Altered Expression and Prospects for Biomarkers
- Amyloid precursor protein trafficking, processing, and function
- Relationship between β-Secretase, inflammation and core cerebrospinal fluid biomarkers for Alzheimer's disease
- Hepatocyte growth factor (HGF/SF) in Alzheimer's disease
- What do people at risk for Alzheimer disease think about surrogate consent for research?
- Meta-analysis of the Association between Alzheimer Disease and Variants in GAB2, PICALM, and SORL1
- Early syndecan-4 upregulation predicts cognitive and pathological trajectories in Alzheimer disease
- Oxidative damage in mild cognitive impairment and early Alzheimer's disease
- Aphasic variant of Alzheimer disease: Clinical, anatomic, and genetic features
- Linkage and mutational analysis of familial Alzheimer disease kindreds for the APP gene region