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 5,209 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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However, the extent to which increasing age, Aβ, and ε4 are associated with memory decline remains unclear, and the age at which memory decline begins for Aβ-positive ε4 carriers and noncarriers has not been determined.
Why it matters
Among 447 participants, memory decline began at an earlier age in amyloid-positive apolipoprotein E ε4 carriers (64.5 years) than in amyloid-positive noncarriers (76.5 years), with larger declines by age 85. This describes how age, amyloid and ε4 combine to affect memory decline and does not provide a treatment or cure.
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66/100
Alzheimer's disease (AD) is the most common cause of dementia.
Why it matters
This is a systematic review of acupuncture for mild to moderate Alzheimer's disease, and it notes that no medical treatment can currently stop or reverse the underlying neurodegeneration. It states that earlier evidence on whether acupuncture improves cognitive function was not strong enough, so this review was set up to examine efficacy and safety.
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APOE ε4 carriage and older age were predictors of longitudinal Aβ accumulation within the Aβ- group but not the Aβ+ group.
Why it matters
In 595 older adults without dementia, APOE ε4 and older age predicted faster buildup of amyloid in those who started without amyloid, while APOE ε2 appeared protective in that group. The authors suggest APOE genotype and age may help select participants for prevention trials, but this study did not test any treatment.
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Cognitive decline is a debilitating manifestation of disease progression in Parkinson's disease.
Why it matters
This study built a clinical-genetic score to predict global cognitive impairment in Parkinson's disease using data from nine cohorts. It is about predicting cognitive decline in Parkinson's disease, not about treating, curing or preventing Alzheimer's disease.
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In clinically normal older adults, lower functional connectivity predicted more rapid decline in PACC scores over time, particularly when coupled with increased Aβ burden.
Why it matters
In clinically normal older adults, lower functional connectivity in the default, salience, and control networks predicted later cognitive decline, and combining this with higher amyloid burden predicted the steepest decline. This suggests resting-state functional connectivity MRI may be useful as a predictor of early Alzheimer-related cognitive decline in research settings.
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ADCOMS is proposed as new standard outcome for pAD and mild AD dementia trials, and is progressing in a CAMD-sponsored qualification process for use in registration trials of pAD.
Why it matters
This study developed a composite clinical outcome score, ADCOMS, from items of established scales, which showed improved sensitivity to clinical decline in prodromal Alzheimer's disease, amnestic mild cognitive impairment, and mild Alzheimer's disease dementia. ADCOMS also detected treatment effects associated with cholinesterase inhibitors, but it is a measurement tool rather than a treatment itself.
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The 52 baseline participants comprised autosomal dominant Alzheimer's disease mutation carriers (n = 11; 49.6 ± 10.3 years old) and non-carriers (n = 16; 51.1 ± 14.2 years old; 10 male), and patients with sporadic mild cognitive impairment (n = 17; 61.9 ± 6.4 years old; nine male) and sporadic Alzheimer's disease (n = 8; 63.0 ± 6.5 years old; five male); for confidentiality reasons, the gender of mutation carriers is not revealed.
Why it matters
In people with autosomal dominant Alzheimer's disease mutations, amyloid plaque deposition and a rise then fall in astrocytosis were seen years before expected symptoms. This describes early brain changes in a rare inherited form, but it does not show how to treat or prevent the disease.
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Within-person changes in CSF biomarkers were also compared with changes in cortical PiB binding and progression to a CDR higher than 0 at follow-up.
Why it matters
This cohort study found that changes in a spinal fluid marker of amyloid begin as early as early middle age and are linked to later amyloid buildup and cognitive decline. It may help identify people at risk earlier, but it does not show that any treatment or prevention works.
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The (11)C-PiB-PET imaging results demonstrated reduction of fibrillar Aβ accumulation in patients with Alzheimer disease treated with bapineuzumab; however, as no clinical benefit was observed, the findings are consistent with the hypotheses that bapineuzumab may not have been initiated early enough in the disease course, the doses were insufficient, or the most critical Aβ species were inadequately targeted.
Why it matters
In two phase 3 trials, bapineuzumab reduced fibrillar amyloid-beta accumulation on PET imaging in APOE ε4 carriers and in pooled analyses, but not in the noncarrier trial separately. This imaging result concerns amyloid burden and does not by itself show that bapineuzumab treats, cures, or prevents Alzheimer's disease.
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At 48 months, group differences between clinical progressors and non-progressors were significant for self (2.13, SE=0.45, P Conclusions and relevance Demonstrating long-term clinical benefit will be critical for the success of recently launched secondary prevention trials.
Why it matters
A questionnaire called the Cognitive Function Instrument detected differences between older people who later showed clinical decline and those who did not over 48 months. This is about tracking early changes for use in prevention trials, not about treating or preventing Alzheimer's disease itself.
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Second, we examined the relevance of Thal amyloid phase in a prospectively-followed autopsied cohort who underwent ante-mortem (11)C-Pittsburgh compound B imaging; using the large autopsy cohort to broaden our perspective of (11)C-Pittsburgh compound B results.
Why it matters
In this autopsy cohort, the Braak tangle stage, but not the Thal amyloid phase, predicted age at onset, disease duration, and final Mini-Mental State Examination score. This suggests that tangle pathology tracked clinical course better than amyloid phase in these cases, but the study was not a treatment trial and offers no direct route to curing or preventing the disease.
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The agreement between Aβ classification with CSF Aβ42 and 18F-flutemetamol positron emission tomography was very high (κ = 0.85).
Why it matters
Spinal-fluid Aβ42 and 18F-flutemetamol amyloid PET classified people's brain amyloid status the same way most of the time (κ = 0.85), and the spinal-fluid level tracked PET amyloid in every cortical region, most strongly in the posterior cingulum and precuneus (r = −0.72). The two tests were not equivalent, though: among people with abnormal amyloid, the PET signal, but not spinal-fluid Aβ42, was associated with global cognition, memory and hippocampal volume. The record does not describe who was studied or the cutoffs used, and agreement with a scan does not show that amyloid testing diagnoses, treats or prevents Alzheimer's disease.
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This Position Paper evaluates the strengths and limitations of the International Working Group research diagnostic criteria and proposes advances to improve the diagnostic framework for Alzheimer's disease.
Why it matters
Proposes the IWG-2 research diagnostic criteria for Alzheimer's disease. Criteria set out how the disease is identified for research, which is separate from treating or preventing it.
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66/100
We examined the impact of physical activity (PA) on longitudinal change in hippocampal volume in cognitively intact older adults at varying genetic risk for the sporadic form of Alzheimer's disease (AD).
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66/100
Researchers conducted a large, two-stage meta-analysis of genome-wide association studies in individuals of European ancestry.
Why it matters
A meta-analysis of 74,046 individuals reporting 11 new susceptibility loci for Alzheimer's disease. Risk loci point to biology worth investigating; they do not by themselves give a treatment or a way to prevent the disease.
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Huperzine A is a Chinese herb extract used for Alzheimer's disease.
Why it matters
This meta-analysis of 20 randomized trials examined the benefits and harms of Huperzine A, a Chinese herb extract, for treating Alzheimer's disease. It reviews existing trial evidence on a treatment but does not establish a cure or prevention.
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Previous studies of Aβ plasma as a biomarker for Alzheimer's disease (AD) obtained conflicting results.
Why it matters
Plasma Aβ measurements had limited value for classifying who had Alzheimer's disease and only modest value for predicting progression over 3 years. The authors suggest that longer follow-up with repeated plasma Aβ measurements might be needed before these tests could be useful.
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The authors sought to identify new susceptibility loci for Alzheimer's disease through a staged association study and by testing suggestive loci reported by the Alzheimer's Disease Genetic Consortium in a companion paper.
Why it matters
Reports common variants at ABCA7, MS4A6A/MS4A4E, EPHA1, CD33 and CD2AP associated with Alzheimer's disease. These associations nominate genes for further work and are not treatments.
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Comprehensive and unbiased meta-analysis of all published and unpublished data from case-control studies for the SORL1 single-nucleotide polymorphisms (SNPs) that had been repeatedly assessed across studies.
Why it matters
This meta-analysis reexamined the association between SORL1 variants and Alzheimer's disease across many case-control datasets. It addresses genetic risk association only and does not show that targeting SORL1 treats, cures, or prevents the disease.
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The findings support the clinical efficacy of CR in early-stage AD.
Why it matters
In this single-blind randomized controlled trial, cognitive rehabilitation significantly improved ratings of goal performance and satisfaction in people with early-stage Alzheimer's disease, while the other two groups did not change. This is a nonpharmacological approach to helping with individually relevant goals, not a treatment that changes the disease course.
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NPTs emerge as a useful, versatile and potentially cost-effective approach to improve outcomes and QoL in ADRD for both the PWD and CG.
Why it matters
Reviewing 179 randomized trials of non-drug therapies, the strongest evidence (Grade A) was for multicomponent caregiver interventions delaying placement in a care facility. This is about managing care and quality of life, not curing or preventing the underlying disease.
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Follow-up case-control association study.
Why it matters
This follow-up case-control study replicated associations between variants in the CLU, CR1, and PICALM genes and late-onset Alzheimer's disease. It is genetic association research and does not test any treatment, cure, or prevention.
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Among the 158 participants who accurately recalled their Alzheimer disease risk assessment 6 weeks after risk disclosure, 75 (47.5%) believed their Alzheimer disease risk was more than 5% points different from the Alzheimer disease risk estimate they were given.
Why it matters
Among 158 people who accurately recalled their genetics-based Alzheimer's disease risk estimate, 47.5% believed their risk was more than 5 percentage points different from what they were told, mostly higher. This is about how people perceive risk information and does not test any treatment, cure, or prevention.
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Impaired glucose regulation is a defining characteristic of type 2 diabetes mellitus (T2DM) pathology and has been linked to increased risk of cognitive impairment and dementia.
Why it matters
In this small trial of 28 adults with glucose intolerance, six months of aerobic exercise improved executive function, fitness, and insulin sensitivity. The study was small and did not test whether exercise prevents or treats Alzheimer's disease.
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This study undertook a two-stage genome-wide association study (GWAS) of Alzheimer's disease involving over 16,000 individuals.
Why it matters
A genome-wide association study reporting variants at CLU and PICALM associated with Alzheimer's disease. An association marks genes worth studying further; it does not show that acting on them treats or prevents the disease.
From across this topic
9 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 9. The same 9 appear here every time.
- Cardiovascular disease and Alzheimer's disease: common links
- Alzheimer dementia in Down's syndrome: the relevance of cognitive ability
- Alzheimer's disease: Recent treatment strategies
- Neural correlates of Alzheimer's disease and mild cognitive impairment: a systematic and quantitative meta-analysis involving 1351 patients
- Early diagnosis of Alzheimer's disease: contribution of structural neuroimaging
- Diabetes, Alzheimer disease, and vascular dementia: a population-based neuropathologic study
- Blood-based biomarkers for detecting Alzheimer's disease pathology in cognitively impaired individuals within specialized care settings: A systematic review and meta-analysis
- Increased cerebral metabolism after 1 year of deep brain stimulation in Alzheimer disease
- Exome sequencing identifies rare damaging variants in ATP8B4 and ABCA1 as risk factors for Alzheimer's disease