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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In the present study, our automated classifier successfully classified FTD clinical subtypes with good to excellent accuracy.
Why it matters
This study used machine learning on brain MRI cortical thickness data to classify individuals into frontotemporal dementia, Alzheimer's disease or cognitively normal categories, with the hierarchical tree achieving 75.8% accuracy. It is a classification study and does not test any treatment, cure or prevention.
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The four emerging CSF biomarkers were significantly elevated in the mutation carriers (n = 235) versus noncarriers (n = 145).
Why it matters
This study measured four emerging cerebrospinal fluid biomarkers in families carrying autosomal-dominant Alzheimer disease mutations and found them elevated in mutation carriers, with some altered very early in the disease time course. It is a biomarker study and does not test any treatment, cure, or prevention.
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A lack of understanding of the causes of attrition in longitudinal studies of older adults may lead to higher attrition rates and bias longitudinal study results.
Why it matters
This study examined factors influencing participant dropout in longitudinal Alzheimer's disease research across 35 centers. It warns that high dropout rates may cause underestimation of dementia prevalence and skew study results.
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Alzheimer's disease is the most common cause of dementia worldwide, with the prevalence continuing to grow in part because of the aging world population.
Why it matters
This review states that treatment for Alzheimer's disease is currently aimed at symptoms, not at curing or preventing the disease. It notes that trials are underway that aim to reduce the production and overall burden of Alzheimer's pathology in the brain.
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The amyloid β subgroups did not differ for any psychobehavioural, cognitive, actigraphy, and structural and functional neuroimaging results after adjustment for age, sex, and level of education More participants positive for amyloid β deposition had the APOE ε4 allele (33 [38%] vs 29 [13%], p 1-42 concentration in CSF significantly correlated with mean 18 F-florbetapir uptake at baseline (r=-0·62, p 1-42 to amyloid β 1-40 (r=-0·61, p 18 F-florbetapir uptake at baseline (mean standard uptake value ratio 1·46 [SD 0·16] vs 1·02 [SD 0·20]), and more were carriers of the APOE ε4 allele (three [75%] of four vs 33 [39%] of 83).
Why it matters
In this longitudinal observational study, amyloid-beta subgroups did not differ on psychobehavioural, cognitive, actigraphy, or structural and functional neuroimaging results after adjustment, though more amyloid-positive participants carried the APOE epsilon4 allele. This describes features of people at risk of Alzheimer disease and does not test a treatment or prevention.
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These findings suggest that patterns of cortical Aβ and tau do not differ in people with PD-CN, people with PD-MCI, and healthy older adults.
Why it matters
This cross-sectional study found that patterns of cortical amyloid and tau did not differ between people with Parkinson disease with normal cognition, people with Parkinson disease with mild cognitive impairment, and healthy older adults. It suggests that Alzheimer's-type amyloid and tau patterns are not the main driver of cognitive differences in Parkinson disease, and it does not test a treatment, cure, or prevention.
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The blood-brain barrier (BBB) is a continuous endothelial membrane within brain microvessels that has sealed cell-to-cell contacts and is sheathed by mural vascular cells and perivascular astrocyte end-feet.
Why it matters
This review describes how breakdown of the blood-brain barrier allows neurotoxic blood-derived material into the brain and can start pathways of neurodegeneration, and it notes the barrier's importance for delivering drugs to the brain. It is a review of mechanisms and does not report any treatment that cures or prevents Alzheimer's disease.
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CSF tau and 18 F-AV-1451 have equal performance in early clinical stages of AD, but 18 F-AV-1451 is superior in the dementia stage, and exhibits close to perfect diagnostic performance for mild to moderate AD.
Why it matters
Comparing tau PET with CSF tau measures in 83 participants, 18F-AV-1451 performed very well for Alzheimer dementia and better than CSF t-tau, p-tau and MRI measures, while in prodromal AD there were no significant differences between CSF tau and the PET measure. These are diagnostic comparisons only and do not indicate any way to treat, cure or prevent the disease.
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Defining the primary cognitive endpoint is a major decision for Alzheimer's disease preventive trials.
Why it matters
This paper describes the 3-year cognitive decline in the placebo group of the MAPT trial, finding that older age, higher brain amyloid, APOE-ε4, low RBC DHA+EPA levels, and higher CDR level were associated with higher risk of cognitive decline. The data are presented to help future prevention trials choose cognitive endpoints and calculate sample sizes.
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Proliferation and activation of microglia in the brain, concentrated around amyloid plaques, is a prominent feature of Alzheimer's disease (AD).
Why it matters
Summarizes evidence on microglia in Alzheimer's disease. Most Alzheimer's risk genes are highly expressed by microglia, and there is evidence both that microglia protect against the disease and that activated microglia can harm neurons, for example by engulfing synapses and worsening tau pathology.
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We report for the first time quantitative data on the plasma levels of p-tau181 in controls and patients with AD and DS, and these data suggest that the plasma p-tau181 is a promising blood biomarker for brain AD pathology.
Why it matters
In small pilot cohorts, plasma p-tau181 was higher in people with Alzheimer's disease and in people with Down syndrome than in controls. This early biomarker work may help diagnosis, but it does not show a treatment, cure, or prevention.
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Mutations in APP, PSEN1, and PSEN2 lead to early-onset Alzheimer disease (EOAD) but account for only approximately 11% of EOAD overall, leaving most of the genetic risk for the most severe form of Alzheimer disease unexplained.
Why it matters
This case-control study searched for rare variants contributing to early-onset Alzheimer's disease, since APP, PSEN1 and PSEN2 mutations explain only about 11% of cases. It is a genetic discovery study and does not report a treatment, cure or prevention.
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The recent development of tau-specific positron emission tomography (PET) tracers enables in vivo quantification of regional tau pathology, one of the key lesions in Alzheimer's disease (AD).
Why it matters
In two separate groups of cognitively normal adults and amyloid-positive people with mild cognitive impairment or Alzheimer's dementia, researchers scored the same tau PET scans ([18F]AV-1451) five ways, from whole-brain averages to Braak-stage regions, and found the methods "yielded similar diagnostic accuracies, which differed between cohorts." The authors conclude whole-brain measures "might be adequate" to detect Alzheimer's-related tau, but that "regional measures covering AD-vulnerable regions may increase sensitivity to early tau PET signal, atrophy and memory decline." It is a single-scan comparison of measurement methods with no sample sizes or accuracy figures in this record, and it does not test any treatment or prevention.
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Neuroimaging has made it possible to measure pathological brain changes associated with Alzheimer's disease (AD) in vivo.
Why it matters
This review sorted brain-scan studies, found through Google Scholar and PubMed searches covering 1985 to June 2016, that used computer classification to tell Alzheimer's disease and mild cognitive impairment apart from other groups. It grouped them by scan type (structural MRI, functional MRI, diffusion imaging, FDG-PET and amyloid-PET) and by the brain features measured, such as hippocampal size, connectivity, glucose use and amyloid burden. The authors conclude these methods "show promise for individualized diagnosis and prediction of clinical progression"; that is promise, not a validated clinical test, and the review concerns diagnosis, not treatment.
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Metabolomics identified key disease-related metabolic changes and disease-progression-related changes.
Why it matters
This metabolomics study found that sphingomyelins and ether-containing phosphatidylcholines were altered in preclinical biomarker-defined Alzheimer's stages, while acylcarnitines and several amines changed in symptomatic stages. These findings identify peripheral metabolic changes that may relate to disease stage, but they do not demonstrate any treatment or prevention.
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Identifying individuals at risk for developing Alzheimer disease (AD) is of utmost importance.
Why it matters
This study developed and validated a polygenic hazard score for quantifying individual differences in age-specific genetic risk for Alzheimer disease, using genotype data from 17,008 cases and 37,154 controls. The authors state that with thorough validation, quantifying inherited genetic variation may prove useful for stratifying risk and as an enrichment strategy in therapeutic trials, but this does not itself treat, cure, or prevent the disease.
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The reliable worsening method produced a cut point only for amyloid PET.
Why it matters
This paper describes methods for defining imaging biomarker cut points for brain aging and Alzheimer's disease, including a proposed cut point for amyloid PET. It does not test a treatment or cure, but aims to standardize how imaging biomarkers are interpreted.
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A national multicentric study was performed in patients with ADEOAD harboring a pathogenic mutation within PSEN1, PSEN2, APP, or a duplication of APP, and a minimal follow-up of 5 years.
Why it matters
In a large French cohort of people with dominantly inherited early-onset Alzheimer's disease, seizures occurred in 47.7% of patients after an average follow-up of 8.4 years. This describes how common seizures are in these inherited forms of the disease and does not test any treatment, cure, or prevention.
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This report describes the public health impact of Alzheimer's disease, including incidence and prevalence, mortality rates, costs of care, and the overall impact on caregivers and society.
Why it matters
This report describes the public health impact of Alzheimer's, including incidence, prevalence, mortality, and costs of care. It does not test any treatment or prevention, so it does not directly change how the disease is treated or cured.
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To assess the value of exosomal miRNAs as biomarkers for Alzheimer disease (AD), the expression of microRNAs was measured in a plasma fraction enriched in exosomes by differential centrifugation, using Illumina deep sequencing.
Why it matters
In a comparison of 35 people with Alzheimer's disease dementia and 35 matched controls, a panel of seven microRNAs from a plasma fraction enriched in exosomes predicted Alzheimer's disease status with 83-89% accuracy. This is a preliminary biomarker study and does not treat, cure, or prevent the disease.
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Accumulation of toxic protein aggregates-amyloid-β (Aβ) plaques and hyperphosphorylated tau tangles-is the pathological hallmark of Alzheimer disease (AD).
Why it matters
This 2015 review sets out the idea that amyloid-β builds up in Alzheimer's because the brain makes more than it clears, and says clearance "seems to be impaired in both early and late forms of AD." It names transport across the blood-brain barrier as the most important exit route, and notes that the glymphatic system, a fluid flow through brain tissue driven by support cells called astrocytes, "might contribute to a larger portion" of clearance than once thought. It summarises others' work rather than adding new data, and it tests no treatment.
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56/100
Our findings suggest that inflammation in the CNS increases in normal aging and is intimately related to markers of neurodegeneration in the preclinical stages of AD and SNAP. sAPPβ and β-secretase activity are not useful diagnostic or staging markers in preclinical AD.
Why it matters
In a single-visit study of spinal fluid from 266 cognitively normal volunteers (median age 58.8), the inflammation marker YKL-40 was higher in people at later preclinical Alzheimer's stages (2-3) and in those with suspected non-Alzheimer pathology than in stages 0 and 1. It also rose with age, so the authors conclude that brain inflammation increases with normal aging and tracks markers of nerve damage early on. Two amyloid-processing measures, sAPPβ and β-secretase activity, did not separate the stages and were judged not useful for staging. These are group associations from one time point, not a diagnostic test or a treatment finding.
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It was one of the genes most strongly associated with risk of Alzheimer's disease in a Belgian cohort.
Why it matters
In a Belgian cohort, a low-frequency ABCA7 variant and predicted loss-of-function mutations in ABCA7 were more common in Alzheimer's disease patients than controls, and ABCA7 expression was reduced in carriers of these mutations. This identifies a genetic risk factor for Alzheimer's disease but does not show that targeting ABCA7 treats, cures, or prevents the disease.
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Progressive cognitive decline in combination with a cerebrospinal fluid biomarker pattern of low levels of amyloid-β1-42 and high levels of total tau and phosphorylated tau is typical of Alzheimer's disease.
Why it matters
By linking the Swedish Dementia Registry with a hospital laboratory database, this study assembled 5,676 people with a clinical dementia diagnosis and a complete set of spinal-fluid measurements of amyloid-β1-42, total tau and phosphorylated tau. It asked how this panel, whose pattern of low amyloid-β1-42 and high tau is "typical of Alzheimer's disease," relates to different dementia diagnoses and to disease severity, because other neurodegenerative disorders "may overlap" with Alzheimer's. It is a diagnostic-biomarker study and does not test any treatment or prevention.
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The past two decades of research into the pathogenesis of Alzheimer disease (AD) have been driven largely by the amyloid hypothesis; the neuroinflammation that is associated with AD has been assumed to be merely a response to pathophysiological events.
Why it matters
This 2015 review argues that inflammation in Alzheimer's, long "assumed to be merely a response" to the disease, is in fact one of its drivers, citing new preclinical (laboratory and animal) and clinical data, and names microglia (the brain's immune cells) and "several cytokines" as potential treatment targets. It also notes that Alzheimer's inflammation mainly involves the innate immune system, unlike multiple sclerosis, so the concept "may need refinement." It is a review of existing evidence, not a new study, and reports no tested 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.
- Clinical syndromes associated with posterior atrophy: early age at onset AD spectrum
- Plasma neurofilament light chain in the presenilin 1 E280A autosomal dominant Alzheimer's disease kindred: a cross-sectional and longitudinal cohort study
- Alzheimer's disease and vascular dementia in developing countries: prevalence, management, and risk factors
- Spatial patterns of cortical thinning in mild cognitive impairment and Alzheimer's disease
- Diagnostic performance and prediction of clinical progression of plasma phospho-tau181 in the Alzheimer's Disease Neuroimaging Initiative
- The temporal trend and distribution characteristics in mortality of Alzheimer's disease and other forms of dementia in China: Based on the National Mortality Surveillance System (NMS) from 2009 to 2015
- Atrophy rate in medial temporal lobe during progression of Alzheimer disease
- A responder analysis of memantine treatment in patients with Alzheimer disease maintained on donepezil
- Inverse association of cortisol serum levels with T-tau, P-tau 181 and P-tau 231 peptide levels and T-tau/Abeta 1-42 ratios in CSF in patients with mild Alzheimer's disease dementia
- Cognitive tasks for evoking the P300 event-related potential in Alzheimer's disease and mild cognitive impairment: A scoping review