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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The protective effect of statin on Alzheimer disease (AD) is still controversial, probably due to the debate about when to start the use of statin and the lack of any large-scale randomized evidence that actually supports the hypothesis.
Why it matters
In this total population-based case-control study in Taiwan, mild-to-moderate Alzheimer disease patients with early statin use had a 0.85-risk of AD progression compared with those without early statin use, a significant association. The authors state that future randomized trial studies can confirm these findings, so this is not yet proof of a treatment effect.
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Risk factors for progression from MCI to probable AD differed in men and women.
Why it matters
In 294 people with mild cognitive impairment followed for a median of about 14 months, risk factors for progressing to Alzheimer's disease differed by sex: in men, severe periventricular white matter hyperintensities and poorer global cognitive function; in women, older age, depressive symptoms and APOE ε4 alleles. The authors suggest these differences may lead to gender-specific prevention or treatment strategies, but no such strategy was tested here.
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Patients with behavioural Alzheimer's disease showed worse memory scores than behavioural variant frontotemporal dementia and did not differ from typical Alzheimer's disease, while executive function composite scores were lower compared to behavioural variant frontotemporal dementia and typical Alzheimer's disease.
Why it matters
This study describes clinical, imaging and pathological features of a behavioural variant of Alzheimer's disease, noting memory dysfunction and high APOE ε4 prevalence. It improves understanding of how Alzheimer's disease can present differently, which may help diagnosis but does not test any treatment, cure or prevention.
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Vascular endothelial growth factor was associated with baseline hippocampal volume (t277 = 2.62; P = .009), longitudinal hippocampal atrophy (t858 = 2.48; P = .01), and longitudinal decline in memory (t1629 = 4.09; P Conclusions and relevance Elevated cerebrospinal fluid VEGF was associated with more optimal brain aging in vivo.
Why it matters
This study found that higher levels of vascular endothelial growth factor were associated with larger hippocampal volume and that it modified the relationship between Alzheimer's disease biomarkers and brain aging outcomes. It is biomarker research and does not test a treatment or cure.
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The temporal relationship of cognitive deficit and functional impairment in Alzheimer's disease (AD) is not well characterized.
Why it matters
Using data from placebo patients in several clinical trials, this analysis found that cognitive decline predicts subsequent functional decline in mild Alzheimer's disease. This suggests that changes in thinking and memory come before changes in daily functioning as the disease progresses.
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This study indicates no benefits for memantine in the long-term treatment and prophylaxis of clinically significant neuropsychiatric symptoms.
Why it matters
Over 24 weeks, memantine and antipsychotics did not differ significantly on function or agitation in people with Alzheimer's disease living in care homes. This trial found no clear advantage of one over the other for these symptoms, and it does not address curing or preventing the disease.
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In a middle-aged, at-risk cohort, a physically active lifestyle is associated with an attenuation of the deleterious influence of age on key biomarkers of AD pathophysiology.
Why it matters
In this middle-aged, at-risk cohort, people who reported being physically active showed less age-related change in amyloid burden, glucose metabolism, hippocampal volume, and some cognitive measures than inactive people. The study was cross-sectional, so it cannot show that physical activity causes these differences or prevents Alzheimer's disease.
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Resting-state functional connectivity magnetic resonance imaging changes with progressing AD severity are similar between ADAD and LOAD.
Why it matters
This cross-sectional imaging study found that loss of functional connectivity in brain networks was similar in inherited and late-onset Alzheimer's disease, and that a model built on one type could predict dementia severity in the other. It does not test any treatment, so it offers no direct path to curing or preventing the disease.
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Clinicopathological evidence suggests that the pathology of Alzheimer's disease (AD) begins many years before the appearance of cognitive symptoms.
Why it matters
In families carrying inherited Alzheimer's mutations, people with no symptoms already had lower spinal-fluid amyloid-β1-42 and higher tau, ptau181 and VILIP-1 about 10 to 20 years before the age their symptoms were expected to begin. When the same people were followed over time, spinal-fluid markers of nerve-cell injury fell after that expected onset age, which the authors suggest may reflect a slowing of acute damage as the disease progresses and say needs to be corroborated. The study shows why biomarkers should be tracked within the same person over time; it did not test any treatment and does not show that one works.
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This report discusses the public health impact of Alzheimer's disease (AD), including incidence and prevalence, mortality rates, costs of care, and overall effect on caregivers and society.
Why it matters
This report describes the public health impact of Alzheimer's disease, including incidence, prevalence, mortality, costs of care, and effects on caregivers and society. It does not test any treatment, cure, or prevention.
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The NIA-AA criteria apply to most MCI subjects in both the community and clinical trials settings; however, a sizeable proportion of subjects had conflicting biomarkers, which may be very important and need to be explored.
Why it matters
In 154 people with mild cognitive impairment from a Minnesota community study, compared with 58 from the ADNI-1 research cohort, the authors found the then "newly proposed" NIA-AA criteria for MCI due to Alzheimer disease "apply to most MCI subjects in both the community and clinical trials settings": 43% of the community sample (55% in ADNI-1) had both amyloid and neurodegeneration. But 29% of the community sample (17% in ADNI-1) had neurodegeneration without amyloid, a group the authors say "may not be on an AD pathway", and 14% (16%) had no abnormal biomarkers. Neurodegeneration "appears to be a key factor in predicting progression relative to amyloid deposition alone", though the record gives no progression rates.
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This roughly 15-year interval where the slope of the amyloid SUVR vs time curve is greatest and roughly linear represents a large therapeutic window for secondary preventive interventions.
Why it matters
Using serial amyloid PET scans, this study found that the rate of amyloid accumulation was low at low baseline levels, peaked around a certain level, and then declined toward zero. This describes how amyloid buildup changes over time and does not test any treatment or prevention.
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A 2-hour infusion of 0.1 to 10 mg/kg ponezumab was well tolerated in subjects with mild-to-moderate AD.
Why it matters
This phase I trial gave single intravenous doses of ponezumab, an anti-amyloid antibody, or placebo to people with mild-to-moderate Alzheimer's. The drug was well tolerated, with no drug-attributed serious adverse events and no new microhemorrhage or vasogenic edema, and its mean half-life was about 6 weeks. Amyloid-β in blood rose with dose and spinal-fluid amyloid-β rose at the highest dose, suggesting the antibody alters amyloid-β levels in the central nervous system.
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We sought to develop and evaluate a composite memory score from the neuropsychological battery used in the Alzheimer's Disease (AD) Neuroimaging Initiative (ADNI).
Why it matters
This study developed and evaluated a composite memory score from the neuropsychological battery used in the Alzheimer's Disease Neuroimaging Initiative. It is a measurement tool for tracking memory, not a treatment, cure, or prevention study.
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Using data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) population, we examined (1) cross-sectional relationships between amyloid deposition, hypometabolism, and cognition, and (2) associations between amyloid and hypometabolism measurements and longitudinal cognitive measurements.
Why it matters
This 2012 study used Alzheimer's Disease Neuroimaging Initiative (ADNI) data from 426 people (126 cognitively normal, 162 early MCI, 85 late MCI, 53 Alzheimer's disease) to compare amyloid PET (florbetapir), brain glucose-use PET (FDG) and cognitive test scores. It reports that 29% of normal participants, 43% with early MCI, 62% with late MCI and 77% with Alzheimer's disease were classed as florbetapir positive, and that in both MCI groups florbetapir was 'negatively associated with concurrent FDG and ADAS-cog'. These are observational associations, not a treatment or prevention finding, and the text alzhub holds does not include the study's results on later cognitive decline.
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Increased WMHs are associated with aging, decreased glucose metabolism, and decline in executive function but do not affect AD-specific pathologic progression, suggesting that the vascular contribution to dementia is probably additive although not necessarily independent of the amyloid pathway.
Why it matters
Cardiovascular risk profiles did not predict progression in CSF β-amyloid, FDG PET uptake, or MRI hippocampal atrophy. Greater white matter hyperintensities were linked to worse executive function and, in normal cognition, faster executive decline and lower FDG uptake, but were otherwise not associated with CSF or MRI biomarkers.
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The study aim was to describe the temporal course of cognitive decline in Alzheimer's disease (AD).
Why it matters
Following 226 people who began cognitively healthy and were later diagnosed with Alzheimer's, this study found thinking skills held steady until about 7.5 years before diagnosis, then declined slowly, and then declined more than 4 times faster in the final 2 years before diagnosis. In those autopsied, the amount of Alzheimer's brain pathology was not strongly related to how fast people declined. It describes the course of the disease and does not test any treatment or prevention.
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This cross-sectional evaluation of the NIA-AA criteria for preclinical AD indicates that the 1-3 staging criteria coupled with stage 0 and SNAP categories classify 97% of CN subjects from a population-based sample, leaving only 3% unclassified.
Why it matters
Testing the NIA-AA research criteria for "preclinical" Alzheimer's on 450 cognitively normal people, using amyloid PET, FDG-PET and hippocampal volume, the authors had to add two categories to place everyone: "stage 0" (normal biomarkers) and "suspected non-AD pathophysiology" (SNAP: normal amyloid but abnormal neurodegeneration markers). At their chosen cutpoints, 43% were stage 0, 16% stage 1, 12% stage 2, 3% stage 3, 23% SNAP and 3% unclassifiable. Because each person was assessed once, the study shows how the categories divide a population, not whether people in them go on to decline, which the authors say still needs longitudinal validation.
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Long-term use of sulfonylureas, thiazolidinediones, or insulin was not associated with an altered risk of developing AD.
Why it matters
In this case-control study, long-term use of metformin was associated with a slightly higher risk of Alzheimer's disease, but there was no consistent trend with more prescriptions. Long-term use of sulfonylureas, thiazolidinediones, or insulin was not associated with an altered risk.
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This study examined a transgenic mouse model in which human tau P301L overexpression was restricted to layer II of the entorhinal cortex (EC-II).
Why it matters
Reports on the spread of tau pathology in a model of early Alzheimer's disease.
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Biomarkers have become increasingly important in understanding neurodegenerative processes associated with Alzheimer disease.
Why it matters
This study used data from the Alzheimer's Disease Neuroimaging Initiative to see whether combinations of brain scans, cerebrospinal fluid markers, cognitive tests, and risk factors could predict progression from mild cognitive impairment to Alzheimer disease. It is about prediction of diagnosis, not about treating, curing, or preventing the disease.
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60/100
Lower plasma β-amyloid 42 and 42/40 levels have been associated with incident dementia, but results are conflicting and few have investigated cognitive decline among elders without dementia.
Why it matters
In older adults without dementia, lower plasma beta-amyloid 42/40 was associated with greater cognitive decline over 9 years, and this association was modified by measures of cognitive reserve. This describes a possible marker of future decline; it does not show that measuring or changing plasma beta-amyloid treats, cures, or prevents Alzheimer's disease.
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These data demonstrate that YKL-40, a putative indicator of neuroinflammation, is elevated in AD and, together with Aβ42, has potential prognostic utility as a biomarker for preclinical AD.
Why it matters
In spinal fluid from a discovery group of 47 and a validation group of 292 people, levels of YKL-40, which the authors describe as a "putative indicator of neuroinflammation", were higher on average in very mild and mild Alzheimer's-type dementia than in cognitively normal controls; blood levels were also higher and tracked the spinal-fluid levels. Among people who started out cognitively normal, the ratio of YKL-40 to amyloid-β42 predicted who went on to develop cognitive impairment about as well as tau/Aβ42 and p-tau181/Aβ42, which the authors called the best spinal-fluid markers known in 2010. The study tests no treatment.
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What is known Herbal medicines have been used in the treatment of behavioural and psychological symptoms of dementia but with variable response.
Why it matters
In this 16-week double-blind placebo-controlled trial, 46 people with probable mild to moderate Alzheimer's disease were given saffron or placebo to assess its efficacy. The text provided does not report the results, so no conclusion about treating, curing, or preventing Alzheimer's disease can be drawn from it.
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Hippocampal atrophy, posterior cingulate and frontal glucose hypometabolism, and white-matter tract disruption are well described early macroscopic events in Alzheimer's disease.
Why it matters
In patients with amnestic mild cognitive impairment, this study found sequential relationships in which baseline hippocampal atrophy was linked to later cingulum bundle and uncinate fasciculus atrophy, which in turn was linked to later decline in cingulate and subgenual metabolism. The findings describe a sequence of brain changes in early Alzheimer's disease, not a treatment.
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.
- Altered expression of genes for amyloid and cytoskeletal proteins in Alzheimer cortex
- Alzheimer precursor protein interaction with the Nogo-66 receptor reduces amyloid-beta plaque deposition
- Release of Alzheimer amyloid precursor derivatives stimulated by activation of muscarinic acetylcholine receptors
- Seizures in dominantly inherited Alzheimer disease
- MR signal abnormalities at 1.5 T in Alzheimer's dementia and normal aging
- Olfactory and other sensory impairments in Alzheimer disease
- Neuropathology of Alzheimer's Disease
- Genome-wide analysis of genetic predisposition to Alzheimer's disease and related sex disparities
- The Validation of Multifactor Model of Plasma Aβ 42 and Total-Tau in Combination With MoCA for Diagnosing Probable Alzheimer Disease
- Promoter mutations that increase amyloid precursor-protein expression are associated with Alzheimer disease