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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Genetic and environmental factors that increase the risk of late-onset Alzheimer disease are now well recognized but the cause of variable progression rates and phenotypes of sporadic Alzheimer's disease is largely unknown.
Why it matters
In brain tissue from 48 Alzheimer disease cases, rapidly progressive disease associated with a low frequency of APOE epsilon4 showed more varied structures of amyloid-beta42 particles. This links different amyloid-beta structures to rates of clinical decline but does not test a treatment or cure.
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The findings support the cross-cultural use of a relatively inexpensive odor identification test as an early biomarker of cognitive decline and AD dementia.
Why it matters
In this community cohort, lower baseline odor identification scores were associated with cognitive decline, and impairment in odor identification was superior to deficits in verbal episodic memory in predicting cognitive decline in cognitively intact participants. The authors suggest such testing may have potential to select or stratify patients in treatment and prevention trials.
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Although altered lipid metabolism has been extensively implicated in the pathogenesis of Alzheimer disease (AD) through cell biological, epidemiological, and genetic studies, the molecular mechanisms linking cholesterol and AD pathology are still not well understood and contradictory results have been reported.
Why it matters
This mendelian randomization analysis found that genetic predisposition to increased blood cholesterol and triglyceride levels was not associated with elevated late-onset Alzheimer disease risk. The authors suggest the observed epidemiological associations could be due to other factors.
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Levels of P-S396-tau, P-T181-tau, and Aβ1-42 in extracts of neurally derived blood exosomes predict the development of AD up to 10 years before clinical onset.
Why it matters
This case-control study found that levels of certain proteins in blood exosomes from nerve cells were higher in people with Alzheimer's disease and could predict the disease up to 10 years before symptoms appeared. This is a potential biomarker for early detection, not a treatment or cure.
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Persons with severe CAA compared with those without CAA were more likely to carry an APOE ε4 allele (64.9% vs 42.8%, respectively; P Conclusions and relevance Being Hispanic and having had a transient ischemic attack-like episode were predictors of CAA in persons with AD.
Why it matters
In people with pathologically confirmed Alzheimer's disease, those with severe cerebral amyloid angiopathy were more likely to carry the APOE epsilon 4 allele than those without it. Being Hispanic and having had a transient ischemic attack-like episode were identified as predictors of this condition.
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A tau/Aβ42 ratio of >0.52 constitutes a robust cerebrospinal fluid Alzheimer profile.
Why it matters
This study compared different combinations of spinal fluid markers and found that a tau/Aβ42 ratio above 0.52 was a robust profile for diagnosis and for predicting decline in people with mild cognitive impairment. It concerns diagnosis and prognosis only, not treating, curing or preventing Alzheimer's disease.
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This should be considered when designing protocols for amyloid-modifying clinical trials.
Why it matters
This longitudinal imaging study found that older age, existing microbleeds, higher amyloid burden and cerebrovascular disease may all raise the risk of new lobar microbleeds in people across the cognitive spectrum. The authors note this should be considered when designing trials of amyloid-modifying treatments.
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Solanezumab, a humanized monoclonal antibody that binds amyloid, failed to improve cognition or functional ability.
Why it matters
Two phase 3 trials (EXPEDITION 1 and 2) randomly assigned 1012 and 1040 people with mild-to-moderate Alzheimer's disease to solanezumab, an antibody that binds amyloid, or placebo every 4 weeks for 18 months. Neither trial showed significant improvement in the primary outcomes, and the authors conclude solanezumab failed to improve cognition or functional ability.
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Tau gene has been consistently associated with the risk of Parkinson disease in recent genome wide association studies.
Why it matters
This study measured total tau, phosphorylated tau [181P], and amyloid beta 1-42 in cerebrospinal fluid from 403 Parkinson disease patients in a clinical trial cohort. It examined these molecules as possible markers of Parkinson disease progression, not as treatments, cures, or prevention for Alzheimer's disease.
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A projected 450,000 older Americans with AD will die in 2013, and a large proportion will die as a result of complications of AD.
Why it matters
This report projects that 450,000 older Americans with Alzheimer's disease will die in 2013, many from complications of the disease. It provides mortality figures only and does not test any treatment, cure, or prevention.
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62/100
This study examined rates of dementia progression as ascertained by the Clinical Dementia Rating Sum of Boxes (CDR-SB) for symptomatic Alzheimer's disease (sAD), and assessed participant characteristics as predictors of CDR-SB progression.
Why it matters
This longitudinal study of 792 participants examined how Alzheimer's disease progressed over time as measured by the Clinical Dementia Rating Sum of Boxes. It is about measuring progression for trial design, not about treating, curing or preventing the disease.
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The emphasis on benefits, rather than losses and difficulties, provides a new dimension to the way interventions for caregivers can be conceptualized and delivered.
Why it matters
This is the published plan, not the results, for two randomized trials that teach family caregivers of people with Alzheimer's disease to find benefits in caregiving, such as "a sense of purpose and personal growth", as a way to ease stress. About 12 hours of benefit-finding training, given in groups or individually at home, was to be compared with psychoeducation and simplified psychoeducation. Caregiver burden, cortisol, depression, well-being and perceived benefits were to be tracked for up to 30 months. Because it contains no outcome data, it cannot show whether the approach helps caregivers; it describes a caregiver-support programme, not a treatment for Alzheimer's disease.
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CLU and MS4A4A eSNPs may at least partly explain the LOAD risk association at these loci.
Why it matters
This study found that certain variants at the CLU and MS4A4A risk loci influence the expression levels of those genes in the temporal cortex of the brain. It supports the idea that some Alzheimer's risk variants work by changing how much nearby genes are turned on or off.
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A condensed protocol for communicating genetic risk for Alzheimer disease achieved similar educational results as an extended protocol in this study.
Why it matters
A condensed protocol using a brochure instead of an in-person session gave similar results to the longer protocol for communicating genetic risk of Alzheimer disease, and it required less clinician time. This is about how risk information is shared with people, not about treating, curing or preventing the disease itself.
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Clinicopathologic correlation studies are critically important for the field of Alzheimer disease (AD) research.
Why it matters
This review of the literature concludes that evidence supports the existence of a specific disease defined by the presence of Aβ plaques and neurofibrillary tangles. It notes that the severity of cognitive impairment correlates best with the burden of neocortical neurofibrillary tangles.
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We used Kaplan-Meier survival analysis to examine the distribution of incident ARIA-E from the start of bapineuzumab treatment and proportional hazards regression models to assess risk factors associated with ARIA.
Why it matters
This retrospective analysis looked at amyloid-related imaging abnormalities (ARIA), a brain-scan side effect, in people with Alzheimer's disease treated with the antibody bapineuzumab. New ARIA-H appeared in 17 patients with ARIA-E (47%) compared with 7 of 177 (4%) without it, and ARIA risk was higher in APOE ɛ4 carriers and at high doses. The authors say this "suggest[s] an association" with changes in amyloid in blood vessels; the record gives no effect sizes for these risk factors, and its note that 13 of 15 patients had more infusions during ARIA-E "without any associated symptoms" does not show that ARIA is harmless.
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Over the coming decades, the aging of the baby boom generation is projected to result in an additional 10 million people with AD.
Why it matters
This report projects that aging of the baby boom generation will add about 10 million people with Alzheimer's disease and notes that the proportion of deaths due to Alzheimer's disease has risen. It does not test any treatment, cure, or prevention.
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Why it matters
Projects how reducing risk factors might change how common Alzheimer's disease is. These are projections built on risk factor data, not trial evidence that reducing those risks prevents the disease.
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Changes in functional connectivity in DLB indicate patterns of activation that are distinct from those seen in AD and may improve discrimination of DLB from AD and cognitively normal individuals.
Why it matters
People with dementia with Lewy bodies had a functional connectivity pattern in the precuneus that was distinct from Alzheimer's disease, and both groups differed from cognitively normal participants. This suggests a brain imaging measure might help tell these two dementias apart, which matters for accurate diagnosis, though it does not address treatment or cure.
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Analysis of cross-sectional data from the AIBL study indicates that plasma apoE levels are altered in AD and correlate with AD pathology level.
Why it matters
Total plasma apolipoprotein E and the apoE4 form were lower in people with Alzheimer's disease and decreased with greater amyloid load on PET imaging. In APOE ε3/ε4 carriers, apoE4 levels fell with disease while apoE3 levels rose, suggesting plasma apoE may reflect disease status.
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Increasing cerebral Abeta deposition with age is the pathobiological phenotype of APOE4.
Why it matters
In 241 people aged 45 to 88 with no memory problems, those carrying more copies of the APOE4 gene variant had more amyloid on brain scans and lower amyloid-beta 42 in spinal fluid, while APOE2 carriers showed no age-related rise in scan amyloid — but neither variant was linked to tau in the spinal fluid of the 168 people tested. Amyloid changes were more common at older ages (elevated scan readings in 0% of 45–49-year-olds versus 30.3% of 80–88-year-olds), and spinal-fluid changes appeared earlier, leading the authors to suggest the fluid test "may" detect amyloid before the scan does. This was a one-time comparison of different people, not a follow-up study, and it tested no treatment or prevention.
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A challenge in developing informative neuroimaging biomarkers for early diagnosis of Alzheimer's disease is the need to identify biomarkers that are evident before the onset of clinical symptoms, and which have sufficient sensitivity and specificity on an individual patient basis.
Why it matters
A pattern of brain atrophy similar to that seen in Alzheimer's disease was detected in cognitively normal older adults and those with mild cognitive impairment, and was associated with cognitive decline. This suggests such patterns could help identify early disease, but it does not offer a way to treat or prevent it.
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The neuropsychologic test battery from the Uniform Data Set (UDS) of the Alzheimer's Disease Centers (ADC) program of the National Institute on Aging consists of brief measures of attention, processing speed, executive function, episodic memory, and language.
Why it matters
This paper describes the standard set of brief thinking and memory tests (attention, processing speed, executive function, episodic memory and language) used across the National Institute on Aging's Alzheimer's Disease Centers, with first results from 3,268 cognitively normal, community-dwelling volunteers who were "relatively well-educated". Age, education and sex all affected test scores, so the authors say future norms must take them into account; norms, including norms for ethnic minority groups, were still a future plan. It is a measurement tool paper, not a study of diagnosis accuracy, treatment or prevention.
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62/100
Unadjusted, SNP RS4420638 within APOC1 was strongly associated with AD due entirely to linkage disequilibrium with APOE.
Why it matters
This genome-wide association study found that a variant near APOC1 was strongly linked to Alzheimer's disease, but this was due entirely to its linkage with APOE. No other new risk genes were confirmed in the reported findings.
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Patients with DLB had an increased risk of mortality vs patients with AD (hazard ratio [HR] 1.88, 95% CI: 1.4 to 2.5).
Why it matters
People with dementia with Lewy bodies had a higher risk of death than people with Alzheimer's disease, but the two groups declined in thinking at similar rates. This is information about disease course and prognosis, not about treating, curing or preventing Alzheimer's disease.
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.
- The Alzheimer Conundrum
- 18F-FDG PET Imaging in Neurodegenerative Dementing Disorders: Insights into Subtype Classification, Emerging Disease Categories, and Mixed Dementia with Copathologies
- NF-κB as a Key Mediator of Brain Inflammation in Alzheimer's Disease
- Alzheimer's Disease Linkage to Real-World Evidence (AD-LINE) Study: Linking Claims Data to Phase 3 GRADUATE Study of Gantenerumab
- Multi-Ancestry Transcriptome-Wide Association Studies of Cognitive Function, White Matter Hyperintensity, and Alzheimer’s Disease
- Italian intersocietal recommendations for restructuring the diagnostic-therapeutic pathway for the implementation and appropriate use of anti-amyloid monoclonal antibodies in Alzheimer’s disease
- Olfactory deficit detected by fMRI in early Alzheimer's disease
- Clinical Factors Associated With Discordant Plasma P-Tau217 and Established Alzheimer Disease Biomarkers
- Mini Mental State Examination and Logical Memory scores for entry into Alzheimer's disease trials
- APP locus duplication causes autosomal dominant early-onset Alzheimer disease with cerebral amyloid angiopathy