Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Highest usefulness score first. Studies without a score come last.
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Plasma neurofilament light (NFL) levels may be a marker of neuronal injury.
Why it matters
This study examined whether plasma neurofilament light chain levels differ among cognitively normal, amnestic mild cognitive impairment and Alzheimer's disease participants. It evaluates a potential biomarker, so it does not provide a treatment, cure or prevention.
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49/100
A major feature of Alzheimer's disease (AD) is the loss of noradrenergic locus coeruleus (LC) projection neurons that mediate attention, memory, and arousal.
Why it matters
Postmortem brain tissue showed that loss of nerve cells in the locus coeruleus occurred early, during the transition from no cognitive impairment to mild cognitive impairment, and was linked to worse cognitive function. This identifies an early site of damage but does not offer a treatment or cure.
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Alzheimer's disease (AD) is the primary cause of age-related dementia.
Why it matters
This review states that despite two decades of investment, no drugs have been shown to alter the course of Alzheimer's disease, and that some drug development has shifted toward early prevention of cellular pathology. It summarizes ongoing research into the amyloid and tau pathways rather than reporting a proven treatment.
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Diagnostic change occurred in 46 patients (79%) having both a previous diagnosis of AD and an amyloid-negative scan (P Conclusions and relevance Amyloid PET in addition to routine assessment in patients with cognitive impairment has a significant effect on diagnosis, diagnostic confidence, and drug treatment.
Why it matters
Adding florbetapir amyloid PET to routine clinical assessment changed diagnosis in some patients, including many who had a previous diagnosis of Alzheimer's disease but a negative scan. The study addresses diagnostic value only and does not show any effect on treating, curing or preventing Alzheimer's disease.
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Recent findings suggest that Alzheimer's disease (AD) is a disconnection syndrome characterized by abnormalities in large-scale networks.
Why it matters
This study found that people with mild cognitive impairment and Alzheimer's disease had abnormal organization of brain networks compared to controls. The findings describe brain changes associated with disease progression but do not test any treatment or prevention.
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Alzheimer disease (AD) represents a genetically heterogeneous entity.
Why it matters
Comparing brain tissue, this study found greater neuritic plaques, neurofibrillary tangles and cerebral amyloid angiopathy in autosomal dominant Alzheimer's disease than in sporadic cases. It describes pathology only and reports no treatment, cure or prevention.
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These results suggest that stakeholders in AD prevention research generally wish to know biological test information about their risk for developing AD to assist in making life plans.
Why it matters
In a survey of cognitively intact at-risk participants in an Alzheimer prevention registry, 80% of those unaware of their ApoE or amyloid PET results wanted to know this information, most commonly to participate in research, arrange personal affairs, prepare family for illness, and move life plans closer. About 15% said disclosure of these test results, if required for a clinical trial, would make them less likely to participate, so this survey addresses attitudes toward testing rather than any treatment, cure, or prevention.
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Neuropsychiatric symptoms, also known as behavioral and psychological symptoms of dementia (BPSD), affect the majority of patients with dementia, and result in a greater cognitive and functional impairment.
Why it matters
This study investigated whether neuropsychiatric symptoms are associated with amyloid deposition on PET scans in elderly people with and without cognitive impairment. It explores a relationship between symptoms and brain amyloid but does not test any treatment or cure.
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Vascular insults can initiate a cascade of molecular events leading to neurodegeneration, cognitive impairment, and dementia.
Why it matters
This review examines how vascular insults and dysfunction of cerebral blood vessels, the neurovascular unit and the blood-brain barrier may contribute to the onset and progression of dementia and Alzheimer's disease. It also discusses potential experimental treatments based on the neurovascular model and questions to be addressed by future studies.
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The SVM can be used in single-subject discrimination and can help the clinician arrive at a diagnosis.
Why it matters
An image-based classifier using gray matter density maps distinguished Alzheimer's disease from behavioral variant frontotemporal dementia with accuracies of 82-88% in single-subject diagnosis. This is a diagnostic tool and does not treat, cure, or prevent Alzheimer's disease.
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The occurrence of obesity, commonly estimated using body mass index (BMI), and the most common late-onset dementia, Alzheimer's disease (AD), are increasing globally.
Why it matters
This review of epidemiologic studies found that midlife overweight and obesity were generally associated with increased dementia risk, while elevated late-life BMI was associated with lower risk. It reports observational associations only and does not show any treatment, cure or prevention.
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Anxiety symptoms in aMCI predict conversion to AD, over and beyond the effects of depression, memory loss, or atrophy within AD neuroimaging biomarkers.
Why it matters
In this study of 376 people with amnestic mild cognitive impairment, greater anxiety severity predicted conversion to Alzheimer disease over a median of 36 months, even after accounting for depression, memory loss, and atrophy. Anxiety was also linked to faster decrease in entorhinal cortex volume, though the association with entorhinal thickness missed significance.
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Alzheimer's disease acknowledged as progressive multifarious neurodegenerative disorder, is the leading cause of dementia in late adult life.
Why it matters
This review describes the hallmark brain changes of Alzheimer's disease and notes that currently available treatments are acetylcholinesterase inhibitors such as rivastigmine, galantamine and donepezil, along with an N-methyl-D-aspartate drug. It reports that research has moved toward therapies aimed at the disease's pathophysiological events, but it presents no new treatment result.
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Accumulation and aggregation of amyloid-β (Aβ) peptides in the brain trigger the development of progressive neurodegeneration and dementia associated with Alzheimer's disease (AD).
Why it matters
This review discusses evidence that impaired amyloid-β clearance, rather than production, likely causes sporadic late-onset Alzheimer's disease, and examines the role of the receptor LRP1 in receptor-mediated endocytosis of amyloid-β. It is a review of clearance mechanisms and does not report any treatment, cure or prevention.
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The relationship between PP and CSF biomarkers is age-dependent and observed only in participants in the fifth and sixth decades of life.
Why it matters
In 177 cognitively normal older adults, higher pulse pressure (the gap between systolic and diastolic blood pressure) was linked to spinal-fluid signs of Alzheimer's: more P-tau and less Aβ1-42. The link was age-dependent, seen only in participants in the fifth and sixth decades of life, and the authors suggest that pulsatile blood flow may be related to amyloid build-up and tau-related neurodegeneration.
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Biomarkers can be used to independently predict coincident AD and DLB pathology, a common finding in amnestic MCI and DAT patients.
Why it matters
In the first 22 Alzheimer's Disease Neuroimaging Initiative autopsies, all patients had a pathological diagnosis of Alzheimer disease but only four had pure Alzheimer disease, with other pathologies commonly present. This is a small autopsy study of diagnosis and biomarker correlates, not a test of any treatment, cure, or prevention.
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Alzheimer's disease (AD) is a devastating disorder of increasing prevalence in modern society.
Why it matters
In this study of 86 patients with mild cognitive impairment followed for two years, combining six EEG biomarkers into a diagnostic index predicted conversion to Alzheimer's disease with 88% sensitivity and 82% specificity. This suggests EEG could serve as a non-invasive and relatively cheap screening tool, but it addresses prediction, not treatment or cure.
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The results suggest that (11)C-PIB binding to Aβ deposits in transgenic mouse brain is highly dependent on the AD model and the structure of its Aβ plaques.
Why it matters
In this longitudinal mouse study, 11C-PIB retention was markedly increased in old APP23 mice with large amyloid deposits, and the authors concluded that PIB binding to amyloid in transgenic mouse brain depends highly on the model and plaque structure. This is animal imaging work and does not establish any treatment, cure or prevention in people.
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The subject groups for model derivation comprised 80 healthy subjects (HS), 36 patients with mild cognitive impairment (MCI) who converted to AD dementia within 18 months, 85 non-converter MCI patients who did not convert within 24 months, and 67 AD dementia patients with baseline FDG PET scan were recruited from the AD Neuroimaging Initiative (ADNI) database.
Why it matters
This study introduced and evaluated a voxel-based method of FDG PET imaging to estimate the probability of Alzheimer's disease in an individual. The method was designed and validated using data from healthy subjects, people with mild cognitive impairment, and Alzheimer's disease dementia patients.
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The purpose of the study was to provide characterization of Mexican Americans who meet criteria for Alzheimer's disease (AD) and mild cognitive impairment (MCI).
Why it matters
Mexican American participants with normal cognition, mild cognitive impairment, or Alzheimer's disease were younger, less educated, scored lower on the MMSE, reported more depression symptoms, and had diabetes more often than non-Hispanic white participants. Age was the only significant risk factor for cognitive dysfunction among Mexican Americans, and the study does not test any treatment, cure, or prevention.
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The aim of this study was to establish a link between periodontal disease and Alzheimer's disease (AD) with a view to identifying the major periodontal disease bacteria (Treponema denticola, Tannerella forsythia, and Porphyromonas gingivalis) and/or bacterial components in brain tissue from 12 h postmortem delay.
Why it matters
This study looked for periodontal bacteria and their components in short-term postmortem brain tissue from 10 Alzheimer's cases and 10 non-Alzheimer's controls, and exposed an astrocyte cell line to P. gingivalis lipopolysaccharide. It is a small tissue and cell study and reports no treatment, cure or prevention for Alzheimer's disease.
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Patients with nonspouse caregivers less frequently participate in AD dementia trials.
Why it matters
This analysis of six Alzheimer's disease clinical trials found that participants with spouse study partners had a lower dropout rate than those with other study partners, and that study partner type was associated with some baseline differences in daily living scores. These findings are about how trials are conducted and do not test any treatment, cure, or prevention for Alzheimer's disease.
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Accumulating evidence suggests that neuroinflammation, mediated by the brain's innate immune system, contributes to AD neuropathology and exacerbates the course of the disease.
Why it matters
In mice, an immune challenge late in pregnancy left the offspring with long-lasting brain inflammation, more APP protein in the hippocampus, abnormal tau, and working-memory problems in old age. Amyloid deposits were not significantly increased in ordinary mice at 15 months, but rose sharply in mice genetically engineered to develop Alzheimer's. The authors suggest systemic infections are "a major risk factor" for Alzheimer's, but this is untested in people and the study tested no treatment.
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Of the 296 initially normal subjects, 31 (10%) progressed to a diagnosis of mild cognitive impairment (MCI) or dementia (27 amnestic MCI, 2 nonamnestic MCI, and 2 non-AD dementias) within 1 year.
Why it matters
In 296 cognitively normal people from the Mayo Clinic Study of Aging, the share diagnosed with mild cognitive impairment or dementia over about a year rose with each preclinical Alzheimer stage: 5% at stage 0, 11% at stage 1, 21% at stage 2 and 43% at stage 3. Most of the 31 people who progressed developed mild cognitive impairment (2 developed non-Alzheimer dementias), and the authors note the follow-up was short. The result supports the staging for grading risk, but it does not predict outcomes for individuals and tested no treatment or prevention.
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Neuropsychological assessment has featured prominently over the past 30 years in the characterization of dementia associated with Alzheimer disease (AD).
Why it matters
This review describes how neuropsychological testing identifies and tracks the cognitive and behavioral symptoms of Alzheimer's disease, often starting with episodic memory. It is about assessment and diagnosis, not about treating, curing, or preventing the disease.
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.
- Familial Alzheimer Dementia: a prevalent disorder with specific clinical features
- Endogenous estrogen levels and Alzheimer's disease among postmenopausal women
- Neurodegeneration in Alzheimer’s Disease: Integrating Mechanism with Translational Therapeutic Strategies
- Neuroinflammation in Alzheimer's disease
- De novo deleterious genetic variations target a biological network centered on Aβ peptide in early-onset Alzheimer disease
- Cerebrospinal fluid tau/beta-amyloid(42) ratio as a prediction of cognitive decline in nondemented older adults
- Association of Kidney Function With Development of Alzheimer Disease and Other Dementias and Dementia-Related Blood Biomarkers
- Physical activity attenuates age-related biomarker alterations in preclinical AD
- Plasmalogen deficiency in early Alzheimer's disease subjects and in animal models: molecular characterization using electrospray ionization mass spectrometry
- Precuneus amyloid burden is associated with reduced cholinergic activity in Alzheimer disease