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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Regional glucose hypometabolism is a defining feature of Alzheimer disease (AD).
Why it matters
This review links reduced glucose metabolism in the brain to decreased O-GlcNAcylation, a modification found on tau and amyloid precursor protein, and notes that increased O-GlcNAcylation protects against tau and amyloid-beta toxicity. It suggests a possible protective role for O-GlcNAc but reports no treatment or cure.
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This article discusses why CSF biomarkers found in normal-pressure hydrocephalus (NPH) can be misleading when distinguishing NPH from comorbid NPH with Alzheimer disease (AD).
Why it matters
This article discusses how cerebrospinal fluid biomarkers in normal-pressure hydrocephalus can be misleading when distinguishing it from comorbid Alzheimer's disease. It does not report any treatment, cure, or prevention for Alzheimer's disease.
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The incidence of dementia is increasing at an alarming rate, and has become a major public health concern.
Why it matters
This review suggests that inflammation, possibly through blood-brain barrier dysfunction, may contribute to both cognitive and non-cognitive symptoms in Alzheimer's disease. The evidence for the blood-brain barrier link comes from experimental mouse models, so it is preliminary and does not yet provide a treatment or cure.
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Alzheimer׳s disease (AD) is the most common cause of dementia in North America.
Why it matters
This mini-review proposes that Alzheimer's disease involves impaired brain insulin responsiveness and glucose use, and suggests the term 'Type 3 diabetes' for these underlying abnormalities. It also discusses whether nitrosamine exposures might contribute, but presents no treatment or cure.
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Resting state functional magnetic resonance imaging (fMRI) was used to measure whole brain functional connectivity within specific networks hypothesised to be more affected in dementia with Lewy bodies (DLB) (a disease characterised by prominent attentional deficits, spontaneous motor features of parkinsonism and depression) than in Alzheimer׳s disease (AD) and controls.
Why it matters
In this small study of 68 people, resting-state fMRI showed lower functional connectivity in several brain networks in dementia with Lewy bodies compared with Alzheimer's disease and controls. It is about distinguishing these dementias using imaging, not about treating or preventing Alzheimer's disease.
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Multiple factors including BPSD, impaired life function and geriatric syndrome were cognitive stage-dependently associated with CB.
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45/100
Both ATH and AD involve inflammation, macrophage infiltration, and occlusion of the vasculature.
Why it matters
This review argues that atherosclerosis and Alzheimer's disease may reflect different manifestations of a common underlying process involving inflammation, macrophages, the vasculature, and amyloid-beta. It is a conceptual discussion and does not report a proven treatment, cure, or prevention for Alzheimer's disease.
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45/100
Processing of the amyloid precursor protein (APP) by γ-secretase results in generation of Aβ peptides of different lengths ranging from 51 to 30 residues.
Why it matters
Using a combined immuno- and LC-MS-based assay under near-native conditions, this work identified intermediate steps in how γ-secretase produces amyloid β peptides of different lengths. It is basic laboratory research and does not show a treatment, cure, or prevention for Alzheimer's disease.
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Alzheimer Disease (AD) is a neurodegenerative disorder and the most common form of dementia.
Why it matters
This review describes the hallmark Alzheimer's pathology of neurofibrillary tangles and neuritic plaques surrounded by activated astrocytes and microglia, and notes that the main plaque component is amyloid-beta peptide. It reports no treatment, cure or prevention finding.
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Astrocytosis shows a distinct regional pattern in AD brain compared to fibrillar Aβ, suggesting that different types of astrocytes may be associated with the pathophysiological processes in AD.
Why it matters
In postmortem Alzheimer brain, binding of tracers for fibrillar amyloid, activated microglia and activated astrocytes was increased in some regions while nicotinic receptor binding was decreased. This is a tissue binding study describing distributions of pathology, not a treatment or prevention result.
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Researchers have begun to characterize the subtle biological and cognitive processes that precede the clinical onset of Alzheimer disease (AD), and to set the stage for accelerated evaluation of experimental treatments to delay the onset, reduce the risk of, or completely prevent clinical decline.
Why it matters
This review describes how Alzheimer's disease is now understood as a sequence of biological changes starting before symptoms appear, and how brain imaging and cerebrospinal fluid measures can detect this preclinical stage. It argues that some therapies may only work if started before clinical symptoms, which has led to a new era of prevention research, but no specific treatment is tested or proven here.
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Amyloid PET imaging is a novel diagnostic test that can detect in living humans one of the two defining pathologic lesions of Alzheimer disease, amyloid-β deposition in the brain.
Why it matters
This paper clarifies and expands appropriate use criteria for amyloid PET imaging, including who counts as a dementia expert and which mild cognitive impairment patients are suitable. It concerns how to use a diagnostic test and does not report any treatment, cure or prevention.
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Advances in AD biomarker research have demonstrated changes in amyloid-beta (Aβ), brain metabolism and other pathophysiologies prior to the onset of memory loss, with some markers possibly changing one or two decades earlier.
Why it matters
This paper proposes that tau damage in the locus coeruleus, the brain's main source of norepinephrine, may be the earliest sign of Alzheimer's and that losing norepinephrine could drive inflammation and reduce amyloid clearance in animal models. It suggests that treatments aimed at amyloid should be given at the earliest detectable stage, such as mild cognitive impairment, or before, but it reports no treatment tested in people.
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The clusters of significant depression and compensation were further used as volumetric regions of interest (ROIs) in a brain interregional correlation analysis in each prodromal AD subgroup to explore metabolic connectivity.
Why it matters
In this imaging study, highly educated patients with prodromal Alzheimer's disease showed more severe hypometabolism in certain left-sided brain regions than poorly educated patients, suggesting they cope better through neural reserve and compensatory networks involving the right dorsolateral frontal cortex. It is an observational imaging finding and does not show that any treatment, cure or prevention works.
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How experienced psychiatrists view the capacity of patients with Alzheimer disease for consenting to research and for appointing a proxy may be related to the patients' conceptualization and memory functioning.
Why it matters
In 77 people with Alzheimer disease, the ability to consent to research and to appoint a research proxy was linked to specific neuropsychological test scores. This is about how capacity is assessed, not about treating, curing, or preventing the disease.
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Alzheimer disease (AD) and frontotemporal lobar degeneration (FTLD) may have overlapping clinical presentations despite distinct underlying neuropathologies, thus making in vivo diagnosis challenging.
Why it matters
This study tested whether MRI volumes could predict cerebrospinal fluid total tau and other biomarkers to help tell Alzheimer's disease from frontotemporal lobar degeneration without a lumbar puncture. It is a diagnostic screening study, so it does not show a treatment, cure or prevention.
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These findings suggest that APOE genotype has a differential effect on the distribution of amyloid plaques and glucose metabolism.
Why it matters
In Alzheimer's dementia patients with abnormal amyloid scans, the number of APOE ε4 copies affected where amyloid and reduced brain glucose use showed up: there was a reversed ε4 dose effect for amyloid in the frontal lobe, while carrying ε4 was linked to more severe metabolic impairment in the back of the cortex. The authors say this differential effect of APOE genotype may have important implications for emerging therapies that aim to intervene directly in the disease process.
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Despite tremendous investments in understanding the complex molecular mechanisms underlying Alzheimer disease (AD), recent clinical trials have failed to show efficacy.
Why it matters
This review proposes that the mechanism causing genetically determined Alzheimer's disease may not be the same as the mechanism causing late-onset Alzheimer's disease, and it suggests a role for chronic inflammation. It offers a hypothesis about late-onset disease but does not report a treatment, cure, or prevention.
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Alzheimer disease (AD) is the most prevalent cause of dementia in humans, and the symptoms are commonly manifested after the seventh decade of life.
Why it matters
This review discusses how reactive astrocytes surrounding amyloid plaques appear to drive the inflammatory process in Alzheimer's disease through release of cytokines and toxic products. It is a discussion of potential translational approaches and does not report any confirmed treatment, cure or prevention.
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Cerebrospinal fluid values of total tau (T-tau) and β-amyloid 1-42 (Aβ 1-42) obtained using the Innotest enzyme-linked immunosorbent assay were transformed using a linear regression model to equivalent values obtained using the INNO-BIA AlzBio3 (xMAP; Luminex) assay.
Why it matters
This study compared cerebrospinal fluid tau and amyloid beta 1-42 values from two different analytical platforms to differentiate Alzheimer disease from frontotemporal lobar degeneration using autopsy-confirmed cases. It is a diagnostic methods study and does not test any treatment, cure, or prevention.
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Biomarker validation in a clinical cohort.
Why it matters
In ten older patients, cerebrospinal fluid levels of Aβ and tau were measured every 6 hours over 24 or 36 hours to see whether they fluctuate significantly. This very small study is about how stable these biomarkers are, not about any treatment or prevention.
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The relation between pathology and cognitive dysfunction in dementia is still poorly understood, although disturbed communication between different brain regions is almost certainly involved.
Why it matters
This small MEG study of 18 Alzheimer patients and 18 healthy controls found changes in brain network modules, with loss of communication between regions related to cognitive impairment. It supports viewing dementia as a network disorder but does not test any treatment, cure, or prevention.
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45/100
APP expression misregulation can cause genetic Alzheimer's disease (AD).
Why it matters
This study investigated whether single nucleotide polymorphisms in the 3'UTR of APP found in Alzheimer's patients affect microRNA function. It is genetic laboratory work and does not test any treatment or show a way to prevent the disease.
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TDP-43 pathology was more frequent in cases with HpScl compared with those without HpScl (89% vs. 24%).
Why it matters
Among 205 dementia patients at autopsy, 14% had hippocampal sclerosis, usually with TDP-43 pathology, and some of these had been mistaken for Alzheimer disease clinically. This is an autopsy study that highlights diagnostic overlap and does not test treatment.
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Increasingly, clinical trials are being planned in patients with mild cognitive impairment (MCI) to prevent or delay the onset of dementia in Alzheimer disease (AD) by disease-modifying intervention.
Why it matters
This study evaluated a quantitative FDG PET score as a biomarker for progression in Alzheimer's disease and mild cognitive impairment. It concerns a biomarker for patient selection and outcome assessment in trials, not a treatment, cure or prevention.
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.
- Quality Gaps in Online Media Coverage of Antiamyloid Monoclonal Antibodies for Alzheimer Disease
- P2‐435: NEIGHBORHOOD DISADVANTAGE IS ASSOCIATED WITH NEUROPATHOLOGICALLY CONFIRMED ALZHEIMER'S DISEASE
- Distinct inflammatory phenotypes of microglia and monocyte-derived macrophages in Alzheimer's disease models: effects of aging and amyloid pathology
- Changes in the Parietal Lobe Subregion Volume at Various Stages of Alzheimer’s Disease and the Role in Cognitively Normal and Mild Cognitive Impairment Conversion
- Accelerated Brain Volume Loss Caused by Anti-β-Amyloid Drugs: A Systematic Review and Meta-analysis
- It's complicated: The relationship between sleep and Alzheimer's disease in humans
- Anxiety and depression in family caregivers of people with Alzheimer disease: the LASER-AD study
- The Alzheimer's Disease Centers' Uniform Data Set (UDS): the neuropsychologic test battery
- Objective physical activity and Alzheimer's disease burden in the population‐based Rotterdam Study
- Is dietary choline intake related to dementia and Alzheimer's disease risks? Results from the Framingham Heart Study