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 5,413 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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In community and clinical settings, SCC predict both dementia and depression in the absence of dementia.
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In this case-control study, blood biomarkers indicative of AD pathology demonstrated different dynamics of change after cardiac arrest.
Why it matters
In people who had out-of-hospital cardiac arrest, serum p-tau rose early in those with poor neurological outcome and then fell, while amyloid-beta levels rose over time in most patients. These Alzheimer-related blood markers changed after cardiac arrest but were only weakly linked to neurological outcome, and the study did not test any Alzheimer treatment.
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We found that the mass spectrometry-based p-tau217 (p-tau217WashU) exhibited significantly better performance than all other plasma p-tau biomarkers when detecting abnormal Aβ status [area under curve (AUC) = 0.947; Pdiff 0.09), but higher compared with AUC of p-tau231UGOT, p-tau181Lilly, p-tau181UGOT, p-tau181Fuji and p-tau181Splex (AUCrange 0.642-0.813; Pdiff ≤ 0.029).
Why it matters
This study compared several blood tests for the protein p-tau in people with mild cognitive impairment. A mass-spectrometry p-tau217 test was best at spotting people with amyloid in the brain (AUC 0.947, against 0.642–0.813 for five other assays) and matched spinal-fluid levels most closely (R = 0.891, against 0.755 for a second p-tau217 test). The authors say the best tests "rival the gold standards of Aβ-PET and CSF" but that the findings need further validation, so it does not establish any blood test as a stand-alone diagnosis.
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Encouraging results were found for several biomarkers, alone or in combination.
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Limbic-predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) and Alzheimer's disease neuropathologic change (ADNC) are each associated with substantial cognitive impairment in aging populations.
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72/100
Apolipoprotein E (ApoE) ε4 genotype was the main risk factor for both ARIA types; ARIA-E incidence was further associated with treatment dose, affecting the 55% of ApoE ε4 carriers in the high-dose aducanumab treatment group.
Why it matters
This review found that amyloid-related imaging abnormalities are common side effects of amyloid-targeting antibody treatments, and that APOE epsilon4 carriers were at highest risk, with 55% of epsilon4 carriers in the high-dose aducanumab group affected. It highlights the need for standardized monitoring, not a cure or prevention.
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72/100
Of 343 participants, the mean (SD) age was 72.56 (7.24) years, and 157 (51.1%) were female.
Why it matters
The available text reports only the age and sex of 343 participants in a cohort study. It provides no information on treating, curing or preventing Alzheimer disease.
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When identifying participants with abnormal CSF Aβ42/40 in the whole cohort, plasma IP-MS-WashU Aβ42/40 showed significantly higher accuracy (area under the receiver operating characteristic curve [AUC], 0.86; 95% CI, 0.81-0.90) than LC-MS-Arc Aβ42/40, IA-Elc Aβ42/40, IA-EI Aβ42/40, and IA-N4PE Aβ42/40 (AUC range, 0.69-0.78; P Conclusions and relevance The results from 2 independent cohorts indicate that certain MS-based methods performed better than most of the immunoassays for plasma Aβ42/40 when detecting brain Aβ pathology.
Why it matters
Comparing eight blood tests for the amyloid-beta 42/40 ratio, this study found that certain mass-spectrometry-based methods identified abnormal cerebrospinal fluid amyloid-beta 42/40 more accurately than most of the immunoassays. It is about improving a diagnostic blood test and does not test any treatment, cure or prevention.
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In this review of 56 RCTs for AD involving 39 575 participants, 23 348 women (59.0%) were included.
Why it matters
This systematic review of 56 trials found that women were included at a lower proportion than in the general Alzheimer's disease population and that few trials reported sex-stratified results. It concerns trial diversity and reporting, not treatment, cure, or prevention.
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72/100
Aerobic exercise has shown inconsistent cognitive effects in older adults with Alzheimer's disease (AD) dementia.
Why it matters
This randomized controlled trial assigned 96 participants with Alzheimer's disease dementia to 6 months of moderate-intensity cycling or light-intensity stretching and followed them for another 6 months. It tested whether aerobic exercise affects cognition but does not establish a treatment, cure, or prevention for the disease.
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The treatment of Alzheimer's disease (AD) in the field of non-pharmacological interventions is a challenging issue, given the limited benefits of the available drugs.
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Whilst cerebrospinal fluid (CSF) and positron emission tomography (PET) biomarkers for amyloid-β (Aβ) and tau pathologies are accurate for the diagnosis of Alzheimer’s disease (AD), their broad implementation in clinical and trial settings are restricted by high cost and limited accessibility.
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Neuroinflammation commences decades before Alzheimer's disease (AD) clinical onset and represents one of the earliest pathomechanistic alterations throughout the AD continuum.
Why it matters
This review brings together earlier gene and protein studies on brain inflammation in Alzheimer's disease. It lists genes found in large genetic studies (TREM2, CD33, CR1, CLU, ABCA7 and others) that are "potentially linked" to inflammation, and it names microglia and astrocytes as "key cellular drivers and regulators" of that process. It is a map for future research toward tailored treatment: it reports no new data, no patients and no treatment result, and it does not show that these genes cause the disease.
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There was a statistically significant increase in the global estimate of cortical tau burden as measured by standardized uptake value ratio (SUVr) from baseline to 18 months in amyloid-β+ but not amyloid-β- subjects (least squared mean change in flortaucipir SUVr : 0.0524 ± 0.0085, P < 0.0001 and 0.0007 ± 0.0024 P = 0.7850, respectively), and a significant association between magnitude of SUVr increase and baseline tau burden.
Why it matters
In this 18-month longitudinal study, cortical tau burden measured by flortaucipir PET increased significantly in amyloid-beta positive but not amyloid-beta negative participants, and both baseline tau and its change were associated with changes in cognitive performance. The authors describe these results as a preliminary characterization of how tau spreads in Alzheimer's disease.
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Among the 1453 participants in the Framingham dementia study sample, the mean (SD) age was 75 (7) years; 792 (54.5%) were female.
Why it matters
In 1,453 dementia-free Framingham Heart Study participants aged 65+ followed for a median of 6 years, each SD increase in log plasma total tau was associated with a 35% higher risk of Alzheimer's dementia (HR 1.35; 95% CI 1.10-1.67), and higher levels were linked to poorer scores on 7 cognitive tasks. Adding it to age and sex improved risk sorting. The authors suggest it "may be used as a biomarker for risk stratification in dementia prevention trials". It is an association across a group, not a diagnostic test for individuals or a treatment target.
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There was no difference in the age (mean [SD], 74.17 [7.96] years), sex (12 women [67%]), or baseline Mini-Mental State Examination score (mean [SD], 19.39 [3.24]) between the crossover (n = 9) and open-label groups (n = 9).
Why it matters
In this small study of young plasma infusion in people with Alzheimer disease, there was no statistically significant difference between the plasma and placebo groups for adverse events, which were mild to moderate. The authors say the results warrant further exploration in larger, double-blinded placebo-controlled trials, so no benefit for treating or preventing Alzheimer's disease has been shown.
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Study objectives To investigate the cumulative effect of five consecutive nights of partial sleep deprivation (PSD) on a panel of cerebrospinal fluid (CSF) biomarkers in healthy adults.
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Neuroinflammation is proposed as one of the mechanisms by which Alzheimer's disease pathology, including amyloid-β plaques, leads to neuronal death and dysfunction.
Why it matters
This systematic review searched Medline, Embase and PsychINFO up to 23 February 2017 for studies that measured markers of microglia, the brain's main immune cells, in post-mortem brain tissue from people with Alzheimer's disease compared with aged people without neurological disease. It found 113 such articles, and its aim was to test whether raised microglia markers are a consistent feature of Alzheimer's brains. It looks only at brain tissue after death and reports no treatment, cure or prevention.
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Cerebral accumulation of amyloid-β is thought to be the starting mechanism in Alzheimer's disease.
Why it matters
In 437 people without dementia from the ADNI research study, researchers measured amyloid in spinal fluid (CSF amyloid-β42) and on florbetapir PET brain scans, then repeated the PET scan after an average of 2.1 years. They asked whether either test picks up abnormal amyloid buildup before the other; the study's title reports that the spinal fluid test does, but the summary held here gives no figures for how much earlier. It is a study about the timing of tests, not about treatment, and it does not show who will go on to develop dementia.
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72/100
The best CSF measures for identifying MCI-AD were Aβ42/total tau (t-tau) and Aβ42/hyperphosphorylated tau (p-tau) (area under the curve [AUC] 0.93-0.94).
Why it matters
In people with mild cognitive impairment who went on to develop Alzheimer's dementia within 3 years, the best spinal-fluid (CSF) measures (Aβ42 divided by total or phosphorylated tau, AUC 0.93–0.94) and amyloid PET (AUC 0.92–0.93) separated them from healthy older adults about equally well; combining the two did not help, and a whole-brain PET reading was as good as regional ones. The findings held in a second cohort using a different assay and tracer, and the authors conclude the choice between CSF and PET "can be based on availability, costs, and doctor/patient preferences". This is a diagnostic comparison that the authors grade as Class III evidence; it says nothing about treatment or prevention, and it was not tested as a screen for people without symptoms.
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72/100
This study showed that subcutaneous etanercept (50 mg/wk) was well tolerated in this small group of patients with Alzheimer disease dementia, but a larger more heterogeneous group needs to be tested before recommending its use for broader groups of patients.
Why it matters
In this small phase 2 trial of 41 patients with mild to moderate Alzheimer disease, etanercept was well tolerated but there were no statistically significant changes in cognition, behavior, or global function. The study was small and the authors note that a larger trial is needed.
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As tau aggregation pathology correlates with clinical dementia in Alzheimer's disease (AD), a tau aggregation inhibitor (TAI) could have therapeutic utility.
Why it matters
This exploratory phase 2 trial tested a tau aggregation inhibitor, methylthioninium, at three doses in mild or moderate Alzheimer's disease. It was an early dose-finding study, and the text provided does not report whether it prevented disease progression.
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Analysis confirmed the association of APOE with earlier AAO (P = 3.3 × 10(-96)), with associations in CR1 (rs6701713, P = 7.2 × 10(-4)), BIN1 (rs7561528, P = 4.8 × 10(-4)), and PICALM (rs561655, P = 2.2 × 10(-3)) reaching statistical significance (P Conclusions and relevance We confirmed an association of APOE (OMIM 107741) variants with AAO among affected participants with LOAD and observed novel associations of CR1 (OMIM 120620), BIN1 (OMIM 601248), and PICALM (OMIM 603025) with AAO.
Why it matters
In 9,162 white people with late-onset Alzheimer's from 14 data sets, the APOE gene was again strongly linked to an earlier age at onset, and variants in CR1, BIN1 and PICALM were also linked to onset age. The study found that all the known risk genes combined shift onset by about as much as APOE but not more, and it says any other genetic effects are "individually likely to be small". It only looked at people who already had the disease, so it shows when symptoms tend to start, not who will get Alzheimer's or how to prevent it.
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A larger number of deaths are attributable to AD dementia in the United States each year than the number (<84,000 in 2010) reported on death certificates.
Why it matters
Following 2,566 older adults for about 8 years, this study estimated that 503,400 deaths among Americans aged 75 and older in 2010 were attributable to Alzheimer's dementia, far more than the fewer than 84,000 reported on death certificates that year. People who developed Alzheimer's dementia had a higher risk of death (hazard ratio 4.30 at ages 75–84, 2.77 at 85+), and the median time from diagnosis to death was 3.8 years. It measures the disease's mortality burden; it does not test any treatment or prevention.
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Present results suggest that repeated cycles of CT in patients with AD treated with ChEIs are associated with benefits in several areas of cognitive function.
From across this topic
10 of the 5,374 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.
- Hemispheric differences in hippocampal volume predict verbal and spatial memory performance in patients with Alzheimer's disease
- BIOMARCADORES PLASMÁTICOS NA DETECÇÃO PRECOCE DA DOENÇA DE ALZHEIMER: UMA REVISÃO SISTEMÁTICA
- Potential cognitive enhancing and disease modification effects of SSRIs for Alzheimer's disease
- Education Research: Online Alzheimer education for high school and college students: A randomized controlled trial
- Sleep Time Estimated by an Actigraphy Watch Correlates With CSF Tau in Cognitively Unimpaired Elders: The Modulatory Role of APOE
- Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer's disease
- A longitudinal study of Alzheimer's disease: measurement, rate, and predictors of cognitive deterioration
- Insulin Resistance and Alzheimer's Disease: Bioenergetic Linkages
- Predicting Alzheimer progression using EEG-based digital twins
- Alzheimer's disease; a review of the pathophysiological basis and therapeutic interventions