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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Alzheimer’s disease (AD) presents a significant global health challenge, necessitating accurate and early prediction methods for effective intervention and treatment planning.
Why it matters
This study developed a machine learning model combining neural processes and a transformer encoder to predict progression among cognitively normal, mild cognitive impairment, and Alzheimer's disease classes using longitudinal data. It does not test a treatment or cure, but it suggests this type of model may improve prediction of disease progression.
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The amyloid cascade hypothesis as the etiological underpinning of Alzheimer disease (AD) is supported by a large body of literature, the most influential of which are genetic studies of the 1980s and 1990s. Other evidence includes the neuropathology of Down syndrome, apparent toxicity of oligomeric amyloid-β (Aβ), interactions with apolipoprotein E, and the analogy of cardiac amyloidosis.
Why it matters
This review argues that the amyloid cascade hypothesis is not well supported, noting that in controlled clinical trials clinical outcome was either marginally positive or similar to placebo. It concludes that Aβ appears neither to drive nor to mitigate the disease process, so it offers no support for amyloid-targeting treatment.
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Recent positive results of three phase III anti-amyloid monoclonal antibody trials are transforming the landscape of disease-modifying therapeutics for Alzheimer's disease, following several decades of failures.
Why it matters
This report discusses debate over whether the benefit measured in three phase III anti-amyloid monoclonal antibody trials represents a clinically meaningful benefit to patients. It notes gaps in understanding clinical meaningfulness that only long-term longitudinal studies can address, and does not itself test any treatment, cure, or prevention.
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Isolated forebrain synaptosomes, rather than total homogenates, from atg7 iKO mice demonstrated accumulation of synaptic proteins, suggesting that the synapse might be a vulnerable site for protein homeostasis disruption.
Why it matters
In mice, turning off autophagy in adulthood disrupted synapse protein balance and caused cognitive impairment, and autophagy problems were also seen in a mouse model of Alzheimer's disease. This is animal research, so it suggests a possible mechanism but does not establish a treatment or cure for people.
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Alzheimer disease (AD) and Alzheimer Disease and Related Dementias (AD/ADRD) are growing public health challenges globally affecting millions of older adults, necessitating concerted efforts to advance our understanding and management of these conditions.
Why it matters
This review describes how blood biomarkers for Alzheimer's disease are being developed as non-invasive and cost-effective tools for diagnosis, prognosis, and monitoring progression. It does not report a new treatment or cure, only the current state of research into these blood tests.
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In total, 147 participants across 21 US sites were invited to participate and 111 provided informed consent.
Why it matters
This study linked claims data to a phase 3 trial of gantenerumab and found relatively high agreement between clinically confirmed Alzheimer's diagnoses and claims data. It is a data-linkage methods study and reports no results on whether gantenerumab treats, cures, or prevents Alzheimer's disease.
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Diagnostic pathways for patients presenting with cognitive complaints may vary across geographies.
Why it matters
This cross-sectional study described how patients with cognitive complaints are diagnosed across six countries and found that biomarker tests like amyloid PET and CSF testing were ordered at low rates. It highlights variability in diagnostic pathways, not any treatment, cure, or prevention of Alzheimer's disease.
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The global population is expected to have about 131.5 million people living with Alzheimer's disease (AD) and other dementias by 2050, posing a severe health crisis.
Why it matters
This paper from the Women's Brain Project describes sex and gender differences in Alzheimer's disease and argues that new approaches to diagnosis, care and patient journeys should be considered. It is a discussion of sex and gender gaps in research and care, not a study of a treatment, cure or prevention.
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This study found that in preclinical AD, overweight and obesity were associated with better verbal memory in women, whereas obesity was associated with worse global cognition among men.
Why it matters
In 387 cognitively unimpaired amyloid-positive participants, sex modified how obesity related to cognition, but there were no significant sex-by-BMI interactions on tau or amyloid PET. This is a cross-sectional observational study and does not test any treatment, cure or prevention.
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46/100
On achieving conformance, sites can justify a claim that brain amyloid burden reflected by the SUVR is measurable to a within-subject coefficient of variation of no more than 1.94% when the same radiopharmaceutical, scanner, acquisition, and analysis protocols are used.
Why it matters
This document describes a profile for standardizing amyloid PET measurements so that results are precise and comparable across sites. It is about imaging standards and does not report any treatment, cure, or prevention.
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Alois Alzheimer first described in a patient "a peculiar severe disease process of the cerebral cortex", people suffering from this pathology have been waiting for a breakthrough therapy.
Why it matters
This review describes Alzheimer's disease as an irreversible, progressive neurodegenerative brain disorder with a long presymptomatic phase, characterized by amyloid-beta deposition and hyperphosphorylated tau accumulation. It discusses a personalized polypharmacology patient-centered approach rather than reporting a specific treatment result.
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Extracellular plaques composed of the hydrophobic peptide amyloid-β and intraneuronal accumulation of the hyperphosphorylated protein tau (p-tau) are pathological hallmarks found in the brains of most people affected by Alzheimer's disease (AD).
Why it matters
This systematic review examined saliva as a possible source of biomarkers for Alzheimer's and Parkinson's disease, since brain hallmarks are hard to measure directly. It is a review of diagnostic markers, so it does not provide a treatment, cure or prevention.
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High-fat diet had a wider array of metabolic, cognitive, and neuropathological consequences in AD and MxD females compared to males.
Why it matters
In mouse models of Alzheimer's disease and mixed dementia, a high-fat diet caused more metabolic, cognitive, and brain pathology consequences in females than males. These are animal findings, so they cannot yet be applied to preventing or treating dementia in people.
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46/100
Since the original description of amyloid-β plaques and tau tangles more than 100 years ago, these lesions have been considered the neuropathological hallmarks of Alzheimer disease (AD).
Why it matters
This review discusses rare individuals who have a high burden of amyloid plaques and tau tangles at autopsy but remain at their cognitive baseline, a state described as resilience. Studying these brains might help explain the link between these lesions and cognitive impairment and point toward disease-modifying treatments.
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Microglia have been identified as key players in Alzheimer's disease pathogenesis, and other neurodegenerative diseases.
Why it matters
This study analyzed over seventy thousand microglia from aged controls and Alzheimer's patients to characterize expression of the markers Iba1, TMEM119 and P2RY12. It is a laboratory marker study and does not test any treatment, cure or prevention for Alzheimer's disease.
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46/100
Adults with Down syndrome (DS) have an exceptionally high frequency of Alzheimer disease (AD) with a wide variability in onset, from 40 to 70 years of age.
Why it matters
Among 232 adults with Down syndrome and Alzheimer disease, later age of hypothyroidism onset was associated with later age of Alzheimer disease onset, while early hypothyroidism onset and the APOE-Ɛ4 allele were each linked to earlier Alzheimer onset. This is an association study and does not show that treating hypothyroidism prevents or delays Alzheimer's disease.
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Cortical thickness from MRI helped predict conversion from mild cognitive impairment to dementia in Parkinson disease at an individual level, with improved performance when integrated with clinical variables. © RSNA, 2021 Online supplemental material is available for this article.
Why it matters
A machine learning model using cortical thickness from MRI helped predict conversion from mild cognitive impairment to dementia in Parkinson's disease. It is a prediction study and reports no treatment or cure.
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Aducanumab is an anti-amyloid-β (Aβ) antibody that achieved reduced amyloid pathology in Alzheimer's disease (AD) trials; however, it is controversial whether it also improved cognition, which has been suggested would require a sufficiently high cumulative dose of the antibody in the brain.
Why it matters
In the APP23 mouse model, this study compared aducanumab with scanning ultrasound and found that ultrasound combined with microbubbles removes amyloid and restores cognition in these mice. This is animal research, and therapeutic ultrasound in humans has only begun to be investigated, so no treatment or cure for people is established.
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In this review, we focus on the emerging roles of microglia in the brain, with particular attention to synaptic plasticity in health and disease.
Why it matters
This review discusses how microglia interact with synapses and modulate plasticity through cytokines and growth factors. It suggests that maintaining these interactions may be relevant to Alzheimer's disease but does not test a treatment or cure.
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These findings suggest that OCT can detect functional and morphologic changes in the retina of carriers of familial Alzheimer disease who are cognitively unimpaired several years before clinical onset, suggesting that OCT findings and retinal vascular parameters may be biomarkers prior to the onset of cognitive decline.
Why it matters
Comparing 10 cognitively unimpaired carriers of the PSEN1 E280A mutation, which causes early-onset familial Alzheimer's, with 10 noncarrier relatives, retinal scans (OCT) showed thinning of the whole retina and several of its layers in carriers. The authors suggest OCT can detect retinal changes several years before symptoms begin, so retinal measures may serve as biomarkers before cognitive decline.
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46/100
Brain structure in later life reflects both influences of intrinsic aging and those of lifestyle, environment and disease.
Why it matters
This study built a deep neural network model from brain MRI scans of healthy people to estimate 'healthy' brain age and then linked the difference between predicted and actual age to many traits in UK Biobank. It is a modeling and association study and does not test any treatment, cure, or prevention for Alzheimer's disease.
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Growing evidence has suggested an association between sleep duration and Alzheimer's disease (AD), but it is unclear if sleep duration is a manifestation of the AD disease process.
Why it matters
This study found that a genetic risk score for Alzheimer's disease was associated with shorter sleep duration in people without dementia. It does not show that changing sleep duration prevents or treats Alzheimer's disease.
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The neurosensory retina emerges as a prominent site of Alzheimer's disease (AD) pathology.
Why it matters
This review describes evidence that the retina shows signs of Alzheimer's disease pathology, including amyloid plaques, hyperphosphorylated tau, neuronal degeneration, retinal thinning, vascular abnormalities and gliosis. It suggests the retina may be a site for noninvasive imaging, but does not report a treatment or cure.
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In 1907, Alois Alzheimer observed, as he quoted, development of "numerous fibers" and "adipose saccules" in the brain of his diseased patient Auguste Deter.
Why it matters
This review discusses how mitochondrial dysfunction, neuroinflammation, amyloid-beta imbalance, and tau tangles contribute to Alzheimer's disease, with a focus on the role of microglia. It summarizes proposed disease mechanisms and does not present a proven treatment, cure, or prevention.
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Alzheimer's disease (AD) is a neurodegenerative disorder and is identified as the most common cause for dementia.
Why it matters
This review states that there is no definitive cure for Alzheimer's disease and that the five FDA-approved drugs are all used for symptomatic treatment. It says disease-modifying therapies that directly address the pathological changes are needed, and that novel drug candidates with various mechanisms are undergoing different stages of drug development.
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.
- Talking during walking: the diagnostic potential of turn dynamics in Alzheimer’s disease, mild cognitive impairment and cognitive aging
- Amyloid PET Quantitation and Centiloid Thresholds in the Diagnosis of Alzheimer Disease: An Individual Participant Data Meta-Analysis
- Plaque-Associated Local Toxicity Increases over the Clinical Course of Alzheimer Disease
- Dependency Grammar Approach to the Syntactic Complexity in the Discourse of Alzheimer Patients
- Biogen to Realign Resources for Alzheimer's Disease Franchise (Aduhelm discontinuation)
- Race modifies the relationship between cognition and Alzheimer's disease cerebrospinal fluid biomarkers
- Distinct lipid mediator profiles in brain and liver tissues in Alzheimer's disease
- Mechanism of amyloid removal in patients with Alzheimer disease treated with gantenerumab
- A comprehensive review on novel opportunities for Alzheimer therapy by targeting BIN1
- A large-scale comparison of cortical thickness and volume methods for measuring Alzheimer's disease severity