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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PET of β-Amyloid plaques (Aβ) using [ 18 F ] florbetaben ( [ 18 F ] FBB) and [ 18 F ] fluorodeoxyglucose ( [ 18 F ] FDG) increasingly aid clinicians in early diagnosis of dementia, including Alzheimer's disease (AD), frontotemporal disease, dementia with Lewy bodies, and vascular dementia.
Why it matters
This retrospective analysis evaluated whether amyloid and FDG PET scans, along with spinal fluid measurements, are clinically useful in managing patients with suspected dementia. It is a diagnostic study and does not test any treatment or cure.
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Alzheimer disease (AD) is the most prevalent neurodegenerative disorder leading to dementia in the elderly.
Why it matters
In a mouse model of Alzheimer disease with amyloid pathology, three-needle electroacupuncture improved cognition, reduced amyloid load and activated TFEB. This is an animal study, and the authors describe the therapy as promising, not as a proven treatment for people.
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44/100
Alzheimer disease (AD) is a chronic neurodegenerative disorder with complex pathophysiology that affects over 50 million people worldwide.
Why it matters
This review reports that clinical outcomes of anti-amyloid-beta antibodies have been unsuccessful and unable to meet their primary endpoints, with similar trends for treatments targeting tau. It reviews recent anti-amyloid passive monotherapies that reached phase 3 trials, including solanezumab.
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Recent functional magnetic resonance imaging studies have demonstrated that moment-to-moment variability in the blood oxygen level-dependent (BOLD) signal is related to age differences, cognition, and symptomatic Alzheimer's disease (AD).
Why it matters
In 321 cognitively normal adults, resting-state BOLD variability, especially in the default mode network, was related to spinal fluid amyloid-β42 and to markers of neurodegeneration, but not to phosphorylated tau-181. This suggests a possible marker of preclinical change, not a treatment, cure or prevention.
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Despite the presumptive common underlying neuropathology of amyloid plaques and neurofibrillary tangles, the 2 groups displayed 2 different patterns of network perturbation, each concordant with the clinical presentation and the anatomy of neurodegeneration.
Why it matters
This small imaging study found that people with amnestic versus aphasic presentations of Alzheimer's disease showed different patterns of brain network disruption despite presumed shared amyloid and tau pathology. It helps explain how the same pathology can produce different symptoms but does not test treatment, cure, or prevention.
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Racial and ethnic differences in Alzheimer's disease (AD) and related dementias are well documented.
Why it matters
This study compared amyloid PET positivity across racial and ethnic groups and found that Whites were more likely to have a positive amyloid PET than other groups. It addresses differences in a diagnostic test result, not treating, curing, or preventing Alzheimer's disease.
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In China, the crude mortality from AD and other forms of dementia increased from 2009 to 2015, but the age-standardized mortality decreased.
Why it matters
This study found that in China, the age-standardized mortality from Alzheimer's disease and other dementias decreased from 2009 to 2015, but the total burden increased due to the growing elderly population. It describes mortality trends and does not evaluate any treatment, cure, or prevention.
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Alzheimer disease (AD) is a progressive neurodegenerative disorder associated with aging and characterized pathologically by the presence of senile plaques, neurofibrillary tangles, and neurite and synapse loss.
Why it matters
This review pulls together redox-proteomics studies (lab work that finds proteins damaged by oxidation) from cell and animal models and from people across stages of Alzheimer's, from pre-clinical AD and mild cognitive impairment to late AD, as well as people with Down syndrome with and without AD. The authors say these studies indicate that oxidative stress driven by amyloid-β(1-42) begins early and is tied to problems in energy metabolism, mitochondria, synapses, inflammation and protein clean-up. Their call for better biomarker imaging and ways to reduce amyloid-β production is a suggestion. The review tested no treatment and reports no patient numbers.
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Establishing a diagnosis of Alzheimer dementia can be challenging, particularly early in the course of the disease.
Why it matters
This review describes imaging signs and artifacts in amyloid PET and notes that preliminary data show amyloid PET findings alter clinical management in patients meeting appropriate use criteria. It concerns interpretation and diagnosis and does not test any treatment, cure or prevention.
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Utilizing the publicly available neuroimaging database enabled by Alzheimer's disease Neuroimaging Initiative (ADNI; http://adni.loni.usc.edu/ ), we have compared the performance of automated classification algorithms that differentiate AD vs. normal subjects using Positron Emission Tomography (PET) with fluorodeoxyglucose (FDG).
Why it matters
A machine learning classification algorithm using FDG-PET distinguished Alzheimer's disease from normal subjects and was also sensitive to Parkinson's disease dementia and dementia with Lewy bodies. This is a diagnostic finding, not a treatment, cure, or prevention.
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Improved prediction of progression to Alzheimer's Disease (AD) among older individuals with mild cognitive impairment (MCI) is of high clinical and societal importance.
Why it matters
A polygenic hazard score, alone and combined with MRI and cognitive measures, was used to predict progression from mild cognitive impairment to Alzheimer's disease. This suggests such combined measures may help identify which people with mild cognitive impairment are more likely to develop Alzheimer's disease.
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The immune system is now considered a major factor in Alzheimer Disease (AD).
Why it matters
This review argues that both brain and peripheral immune components, such as complement, microglia, monocytes and lymphocytes, contribute to Alzheimer's disease and could be future therapeutic targets. It is a summary of an emerging perspective and reports no treatment that has been shown to cure or prevent the disease.
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Currently, 3 amyloid PET tracers are approved and commercially available for clinical use.
Why it matters
This review reports that amyloid imaging changes diagnosis in about 30% of cases and management in about 60% of cases, with initial simulation studies pointing to a potential positive effect on patient outcome and cost effectiveness. It states these features require confirmation in prospective clinical trials and does not show any treatment, cure or prevention.
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In Alzheimer disease (AD) inflammation becomes evident throughout the course of the disease.
Why it matters
In 27 Alzheimer's dementia patients and 18 controls, this study analyzed a panel of inflammatory cytokines and their relationship to cerebrospinal fluid biomarkers. It is a small observational study of inflammation and markers, not a treatment, cure, or prevention for Alzheimer's disease.
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Cerebral blood flow (CBF) alterations and amyloid-β (Aβ) accumulation have been independently linked to cognitive deficits in older adults at risk for dementia.
Why it matters
This study examined whether cerebral blood flow and amyloid-β status interact to affect memory performance in 62 cognitively normal older adults from the Alzheimer's Disease Neuroimaging Initiative. It is a small observational study, so it cannot show that changing blood flow or amyloid would prevent or treat Alzheimer's disease.
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Hyperphosphorylated tau protein deposits and, inflammatory processes are characteristic components of Alzheimer disease (AD) pathology.
Why it matters
In autopsy brain tissue from three Alzheimer patients and one control, tau tracer binding and activated astrocyte tracer binding showed similar laminar cortical patterns. This is a small in vitro tissue study describing pathology distribution, not a treatment, cure or prevention.
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Alzheimer's disease (AD) is a neurodegenerative condition characterized by the formation of amyloid-β plaques, aggregated and hyperphosphorylated tau protein, activated microglia and neuronal cell death, ultimately leading to progressive dementia.
Why it matters
This short review focuses on neuroinflammation in Alzheimer's disease and the participation of microglia and other factors in neurodegeneration. It reports no treatment, cure, or prevention.
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Alzheimer's disease (AD) is the most common neurodegenerative disorder, neuropathologically characterized by aggregates of β-amyloid peptides, which deposit as senile plaques, and of TAU protein, which forms neurofibrillary tangles.
Why it matters
This review states that neuroinflammation is implicated in Alzheimer's disease and that cytokines and chemokines can affect amyloid precursor protein expression and processing and can influence kinases that phosphorylate TAU. It notes there is still no cure for the disease, and it describes possible therapeutic approaches rather than a proven treatment.
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Laboratory-specific reference values for cerebrospinal fluid (CSF) Alzheimer disease (AD) biomarkers are necessary.
Why it matters
This study measured CSF Alzheimer's biomarkers in Korean patients and recalculated diagnostic cutoff values for that population. It addresses how to diagnose Alzheimer's accurately in a specific group, not how to treat or prevent it.
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The series of events underlying the pathogenesis of Alzheimer disease (AD) in unknown.
Why it matters
This review discusses mitochondria-associated ER membranes and notes that Alzheimer's disease involves features such as altered cholesterol, phospholipid and calcium metabolism and mitochondrial dysfunction alongside plaques and tangles. It is a discussion of possible mechanisms and does not report a treatment, cure or prevention.
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While histological changes in microglia have long been recognized as a pathological feature of Alzheimer's disease (AD), recent genetic association studies have also strongly implicated microglia in the etiology of the disease.
Why it matters
This review discusses microglial genes such as APOE, TREM2, CD33, GRN and IL1RAP as possible entry points for therapeutic intervention and notes that microglia may affect amyloid beta and tau immunotherapy. It is a discussion of considerations rather than a study showing any treatment, cure or prevention.
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It is known that Alzheimer's disease (AD) influences the temporal characteristics of spontaneous speech.
Why it matters
This article summarizes evidence that temporal characteristics of spontaneous speech, such as speech tempo and pauses, may enable a simple early linguistic screening for Alzheimer's disease. It proposes a screening approach, not a treatment, cure, or prevention.
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Brain 18F-FDG PET scans interpreted with Neurostat and 3D-SSP displays accurately detected Alzheimer disease in patients with primary progressive aphasia or corticobasal syndrome as focal-onset dementias.
Why it matters
This study found that 18F-FDG PET imaging diagnosed Alzheimer's disease with 84% accuracy in patients with primary progressive aphasia or corticobasal syndrome. It is a diagnostic accuracy study, not a treatment trial, so it does not show whether any therapy works or prevents Alzheimer's.
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Alzheimer disease (AD) is a neurodegenerative disease with many known pathological features, yet there is still much debate into the exact cause and mechanisms for progression of this degenerative disorder.
Why it matters
This review describes how a method called redox proteomics has identified specific brain proteins that are oxidized in Alzheimer's disease and mild cognitive impairment, supporting a role for oxidative stress in disease progression. It reports laboratory findings only and does not test any treatment, cure, or prevention in patients.
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Neurodegenerative diseases are a major cause of cognitive impairment and can ultimately lead to dementia.
Why it matters
This study found that genetic risk scores for neurodegenerative diseases were associated with mild cognitive impairment and conversion to dementia in a population-based sample. It suggests that genetic information may help identify people at higher risk, but it does not show that treating or changing these genes can prevent dementia.
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.
- Association of Platelet Aggregation With Markers of Alzheimer Disease Pathology in Middle-Aged Participants of the Framingham Heart Study
- Plasma p-tau181 Level Predicts Neurodegeneration and Progression to Alzheimer's Dementia: A Longitudinal Study
- Altered serum glycomics in Alzheimer disease: a potential blood biomarker?
- Correlation between insulin-degrading enzyme versus total tau and selected cytokines in patients with Alzheimer´s disease compared to non-demented controls
- Performance of Alzheimer Disease Plasma Biomarkers in a Specialty Memory Clinic (S15.005)
- Generalizability of tau and amyloid plasma biomarkers in Alzheimer's disease cohorts of diverse genetic ancestries
- The Link Between Physical Activity and Cognitive Dysfunction in Alzheimer Disease
- Alzheimer's Disease: The Role of Microglia in Brain Homeostasis and Proteopathy
- The Utility of Cerebral Blood Flow as a Biomarker of Preclinical Alzheimer's Disease
- Observational studies in Alzheimer disease: bridging preclinical studies and clinical trials