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 is characterized by degenerative changes in a variety of neurotransmitter systems.
Why it matters
This paper describes degenerative changes in neurotransmitter systems and selected brain regions in Alzheimer's disease and how these may underlie aspects of dementia. It is a descriptive account and provides no treatment, cure or prevention.
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Considerable evidence now indicates that Alzheimer's disease (AD) is primarily a vascular disorder.
Why it matters
This review argues that Alzheimer's disease is primarily a vascular disorder and should be reclassified as such, based on evidence such as shared risk factors with vascular dementia and overlapping pathology. It is a proposal about classification and treatment targets, not a proven treatment or cure.
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Acetylcholinesterase inhibitors may be helpful in reversing the symptoms of dementia during early and middle stages of cognitive decline.
Why it matters
In this small pilot study of 6 treated patients with Down syndrome and Alzheimer disease compared with 9 historical controls, dementia scores improved significantly over 3 to 5 months on donepezil. The authors call for a larger study, so this is preliminary evidence about symptom treatment, not a cure or prevention.
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Tumor necrosis factor (TNF) is an important proinflammatory cytokine that is upregulated in Alzheimer disease (AD) patients and involved with AD genes.
Why it matters
This work reports associations between Alzheimer disease and variants in the TNF gene and the TNFR2 receptor gene, but found no significant association with TNFR1. It provides evidence about possible disease mechanisms, not a treatment, cure or prevention.
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Activated astrocytes, overexpressing the neurotrophic signaling molecule S100beta, are invariant components of the Abeta plaques of Alzheimer's disease.
Why it matters
This review proposes that activated astrocytes overexpressing S100B are involved in the evolution of amyloid plaques and neuritic pathology in Alzheimer's disease. It is a mechanistic discussion and reports no treatment, cure or prevention.
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42/100
The clinical impact of Alzheimer's disease pathology at biopsy was investigated in 56 cognitively impaired patients undergoing shunt surgery for idiopathic normal pressure hydrocephalus (NPH).
Why it matters
This study investigated the prevalence of Alzheimer's disease pathology at biopsy and shunt response in patients with idiopathic normal pressure hydrocephalus. It concerns surgical outcomes in a specific patient group and does not test treating, curing or preventing Alzheimer's disease itself.
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Two major risk factors for late-onset familial and sporadic Alzheimer disease (AD), a leading cause of dementia worldwide, are increasing age and inheritance of the epsilon4 allele of the apolipoprotein E gene (APOE4).
Why it matters
In postmortem brain tissue, reducible 4-hydroxynonenal adducts were increased in the hippocampus, entorhinal cortex, and temporal cortex of Alzheimer's patients, and the pattern of accumulation was related to APOE genotype. This links lipid peroxidation to Alzheimer's pathology in an APOE-dependent manner, but no treatment is tested.
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42/100
A key pathological feature of Alzheimer's disease is the formation and accumulation of amyloid fibres.
Why it matters
This laboratory study examined how phosphatidylinositol and inositol affect the growth and stopping of amyloid-beta fibrils. It is basic chemistry work and does not show any treatment, cure or prevention for Alzheimer's disease.
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1H-MRS showed significantly lower N-acetylasparatate concentration in DAT and AAMI compared with controls.
Why it matters
This very small study of 18 people used MRI, SPECT and spectroscopy to compare brain findings in normal aging, age-associated memory impairment and Alzheimer-type dementia. It describes differences that may help distinguish these conditions but does not test any treatment, cure or prevention.
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We conducted an open-label study designed to assess the effects of tacrine on behavioral changes in patients with Alzheimer's disease (AD).
Why it matters
In this open-label study, 28 patients with Alzheimer's disease received tacrine and their behavioral symptoms and cognition were assessed. The open-label design without a control group means these preliminary results cannot establish whether tacrine is an effective treatment.
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The genetics of Alzheimer disease (AD) are complex and not completely understood.
Why it matters
This review of Alzheimer's genetics notes that APP mutations cause early-onset autosomal dominant disease but account for 5% or less of all early-onset familial cases, with a chromosome 14 locus responsible for other families. It is a genetic overview and does not itself provide a treatment, cure, or prevention.
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Seven female patients with mild to moderate dementia of the Alzheimer type (DAT) were treated with long-term, low-dose estrogen replacement therapy (ERT) over a period of 5-45 months.
Why it matters
This report describes seven women with mild to moderate Alzheimer's disease who received long-term low-dose estrogen replacement therapy. It is a small case series with no control group, so it cannot show whether the treatment works.
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Phospholipase A2 (PLA2) is a key-enzyme in the metabolism of membrane phospholipids.
Why it matters
In post-mortem brains, phospholipase A2 activity was decreased in Alzheimer's disease compared with controls. This describes a biochemical difference in brain tissue and reports no treatment, cure or prevention.
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42/100
Here we review current evidence in support of the cortical disconnection/cortical connectivity model of Alzheimer disease (AD) pathogenesis, a model which predicts that one of the first events in AD is damage to the entorhinal cortex and/or subiculum resulting in the disconnection of the hippocampal formation and neocortex, and the subsequent progression of the disease in a stepwise fashion along cortico-cortical connections.
Why it matters
This review proposes a model in which Alzheimer disease begins with damage to the entorhinal cortex or subiculum that disconnects the hippocampus from the neocortex, then spreads along connections. It is a hypothesis-generating review and does not test any treatment, cure, or prevention.
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42/100
The A4 or beta protein is a peptide that constitutes the major protein component of senile plaques in Alzheimer disease.
Why it matters
This study found that a synthetic 42-residue amyloid-beta peptide accumulates inside cultured human skin fibroblasts and remains stable for at least 3 days. It is laboratory research and does not test any treatment, cure, or prevention.
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The early literature on Alzheimer Dementia (AD) describes the clinical features aphasia, apraxia and agraphia as characteristic.
Why it matters
This older study found that language disorder and apraxia were common in Alzheimer's dementia and predicted familial aggregation of dementia, suggesting a distinct clinical entity called Familial Alzheimer Dementia. It addresses clinical identification and family risk, not treatment, cure, or prevention.
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A brief description is given of neurofibrillary changes of the paired helical filament type in a variety of chronic neurological diseases.
Why it matters
This paper describes tangled nerve cell changes of the paired helical filament type in several chronic neurological diseases, including Down syndrome. It is a descriptive report and does not test or propose a treatment or cure for Alzheimer's disease.
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Amyloid-targeted monoclonal antibody therapies have introduced a new era in the treatment of early Alzheimer disease.
Why it matters
A panel of experts concluded that AI-assisted detection of ARIA on MRI is likely to improve patient safety when used as decision support with a radiologist still reviewing the scans. They supported only conditional use with radiologist oversight, ongoing quality assurance, and prospective monitoring, and noted that more studies are needed to show whether better detection actually improves patient outcomes.
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41/100
Introdução: A Doença de Alzheimer (DA) é uma das principais causas de demência em todo o mundo, prejudicando a vida de milhões de pessoas.
Why it matters
This integrative review analyzes scientific evidence on the use of blood biomarkers for early diagnosis of Alzheimer's disease. It is about diagnosis, not treatment, and does not demonstrate any cure or prevention.
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Este ensayo tiene como objetivo analizar la eficacia del lecanemab como terapia modificadora de la enfermedad de Alzheimer (EA).
Why it matters
This literature review aims to analyse the efficacy of lecanemab as a disease-modifying therapy for Alzheimer's disease. No results or conclusions are provided in the available text.
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41/100
Older adults with Alzheimer's disease (AD) frequently present to emergency departments (EDs) with multiple coexisting conditions.
Why it matters
This cross-sectional analysis of emergency department visits identified different patterns of coexisting conditions in people with Alzheimer's disease by age group. It describes emergency presentations and multimorbidity, not any treatment, cure, or prevention.
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ε4 noncarriers and those with lower baseline amyloid burden.
Why it matters
This single-site real-world report describes lecanemab safety and effectiveness, noting two peaks of ARIA-E at about 10 and about 25 weeks that support ongoing MRI monitoring. No marker reliably predicted ARIA, and the authors call for better markers to optimize cognitive outcomes.
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41/100
A total of 51 patients with AD, age (median: 73 years) and 53 cognitively normal subjects (median age: 69) were included.
Why it matters
In 51 patients with AD and 53 cognitively normal subjects, global cerebral blood flow did not differ between groups, but perfusion at the cortical-CSF interface was significantly lower in AD and contributed most to predicting AD probability. The authors state that further validation against established biomarkers of CSF dynamics and clearance pathways is warranted, so this is an early imaging marker finding, not a treatment or cure.
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Anti-amyloid immunotherapy agents represent a novel and clinically significant class of humanized monoclonal antibodies designed to selectively bind and clear pathological amyloid-beta (Aβ) aggregates from the brain, thereby slowing the progression of early Alzheimer’s disease (AD).
Why it matters
This review describes anti-amyloid immunotherapy agents as humanized monoclonal antibodies that bind and clear pathological amyloid-beta aggregates from the brain, thereby slowing progression of early Alzheimer's disease. It covers regulatory considerations including amyloid biomarker confirmation and ARIA risk management for a New Drug Submission to Health Canada.
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Among 5757 participants (21.7% Black, 20.3% Latinx, 58.1% AORE), we found lower odds of amyloid positivity in Black (odds ratio [OR]: 0.72, 95% confidence interval [CI]: 0.62-0.83) and Latinx (OR: 0.78, 95% CI: 0.67-0.91) compared to AORE.
Why it matters
This study found that amyloid PET scans were less often positive in Black and Latinx participants and more often positive in people from more deprived neighborhoods. It does not test any treatment, but the authors note the findings may matter for anti-amyloid therapies.
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.
- Advanced convolutional neural network with attention mechanism for Alzheimer's disease classification using MRI
- Association of cerebrovascular reactivity and Alzheimer pathologic markers with cognitive performance
- Oxidative damage and protection by antioxidants in the frontal cortex of Alzheimer's disease is related to the apolipoprotein E genotype
- Sarcopenia and Muscle Functions at Various Stages of Alzheimer Disease
- Cerebral amyloid angiopathy and its relationship to Alzheimer's disease
- Strategic subcortical hyperintensities in cholinergic pathways and executive function decline in treated Alzheimer patients
- Does caffeine intake protect from Alzheimer's disease?
- Divergent patterns of cognitive decline in preclinical Alzheimer's disease: Implications for secondary prevention trials
- Redox proteomics and amyloid β-peptide: insights into Alzheimer disease
- Systematic review: fluid biomarkers and machine learning methods to improve the diagnosis from mild cognitive impairment to Alzheimer's disease