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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Alzheimer's disease is the most common cause of dementia in elderly people.
Why it matters
This review discusses the successes and failures of Alzheimer's disease clinical trials and drug development. It states that a single cure is unlikely and that drug development approaches need reconsideration, but it does not report a new treatment or cure.
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Furthermore, neuroimaging analysis identified 2 additional loci of high interest for further study.
Why it matters
Markers at the APOE locus were associated with several brain imaging measures in Alzheimer disease, and two additional loci were identified as being of high interest for further study. The findings link known Alzheimer risk loci to brain imaging features but do not establish a treatment or prevention.
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We propose a new method of measuring atrophy of brain structures by simultaneously segmenting longitudinal magnetic resonance (MR) images.
Why it matters
This paper proposes a new 4D graph-cut segmentation method to measure hippocampal atrophy on longitudinal MRI scans. It is a measurement method and does not test any treatment, cure, or prevention.
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Dramatic increases in the numbers of "oldest old" (aged 85 years and older) across all racial and ethnic groups will also significantly affect the numbers of people living with AD.
Why it matters
This report projects that growing numbers of the oldest old will substantially increase the number of people living with Alzheimer's disease. It is a population estimate and does not test any treatment, cure, or prevention.
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Preclinical AD as detected by PET PiB is not benign, as it is associated with progression to symptomatic AD.
Why it matters
In cognitively normal older adults, higher Pittsburgh Compound B binding in the brain predicted progression to very mild dementia of the Alzheimer type. This suggests amyloid imaging may help identify people at higher risk before symptoms appear, though it does not show that treating amyloid prevents dementia.
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Cerebrospinal fluid (CSF) levels of Abeta peptide 1-42 (Abeta 42), tau, and phosphorylated tau (ptau) are potential biomarkers of Alzheimer disease.
Why it matters
This retrospective analysis examined whether cerebrospinal fluid levels of Abeta 42, tau, and phosphorylated tau predict the rate of cognitive change in people with very mild Alzheimer type dementia. It is about biomarkers and prediction of decline, not about treating, curing, or preventing the disease.
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There is a clear need to develop an objective diagnostic test for Alzheimer disease (AD).
Why it matters
CSF changes in Alzheimer's were already "well documented", but the authors noted that how they relate to changes in the brain itself "is not established". This cross-sectional study of 123 patients (79 clinically diagnosed with Alzheimer's, 29 with other dementias, 15 with other neurological diseases) compared spinal-fluid Aβ42, total tau and phosphorylated tau measured in life with Alzheimer-type changes in the brain. The summary we hold ends before the results, so check the original paper for what it found. As a measurement study, it says nothing about treatment or prevention.
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In mostly small single-center studies, Alzheimer's disease (AD) is associated with characteristic and progressive reductions in fluorodeoxyglucose positron emission tomography (PET) measurements of the regional cerebral metabolic rate for glucose (CMRgl).
Why it matters
Using baseline FDG PET images from the Alzheimer's Disease Neuroimaging Initiative, this study compared cerebral glucose metabolism in 74 probable Alzheimer's disease patients and 142 amnestic mild cognitive impairment patients with 82 cognitively normal controls. It is a biomarker and imaging analysis, not a treatment, cure or prevention study.
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60/100
In this review, the evidence that single clinically defined cardiovascular risk factors are significantly associated with incident AD is inconsistent at best.
Why it matters
In this review, single clinically defined cardiovascular risk factors such as hypertension and diabetes were not significantly associated with increased risk of incident Alzheimer's disease. APOE ε4 was the most consistent risk factor, and interactions between risk factors appeared to modify risk.
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A plethora of reports suggest that copper (Cu) homeostasis is disturbed in Alzheimer's disease (AD).
Why it matters
In this small phase 2 trial, copper supplementation had no effect on cognitive performance in people with mild Alzheimer's disease, although it changed one spinal fluid marker. This does not show that copper treats or prevents Alzheimer's disease.
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We used a sensitive and specific beta-site amyloid precursor protein (APP)-cleaving enzyme 1 (BACE1) assay to determine the relationship between BACE1 activity in cerebrospinal fluid (CSF) and markers of APP metabolism and axonal degeneration in early and late stages of Alzheimer disease (AD).
Why it matters
This case-control and follow-up study measured BACE1 activity in cerebrospinal fluid of people with Alzheimer's disease, mild cognitive impairment, and normal controls. It is a biomarker study and does not test any treatment, cure, or prevention.
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APOE epsilon 4 may influence rate of cognitive decline most significantly in the earliest stages of Alzheimer disease.
Why it matters
In population-based and clinic-based samples, the presence of at least one APOE epsilon4 allele was associated with faster cognitive decline in the incident population-based Alzheimer disease group, with parallel results in prevalent samples only after adjustment or exclusions. The findings suggest APOE epsilon4 may influence rate of decline most in the earliest stages, but no treatment was tested.
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Interestingly, we found no consistent differences in learning and memory performance between high versus low PiB cognitively normal or amnestic MCI subjects.
Why it matters
This study found that PiB imaging of amyloid and structural MRI of grey matter loss provide complementary information in Alzheimer's disease and amnestic mild cognitive impairment, and that MRI correlated more strongly with cognitive testing than PiB. It does not test a treatment or cure, but helps clarify the roles of these imaging methods.
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To be diagnostically useful, structural MRI must reliably distinguish Alzheimer's disease (AD) from normal aging in individual scans.
Why it matters
This 2008 study trained a computer method (linear support vector machines) on grey-matter MRI scans and correctly classified "up to 96% of pathologically verified AD patients" versus cognitively normal older people, and 89% of people with mild, clinically probable Alzheimer's versus age/sex-matched controls. A classifier trained on one centre's scans also separated Alzheimer's from normal ageing on another centre's scanner, and the method assigned 89% of autopsy-confirmed cases to Alzheimer's or frontotemporal lobar degeneration. The record gives no group sizes, and it is a diagnostic-method study, not a treatment or prevention finding.
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The predictive validity of mild cognitive impairment (MCI) for identifying future Alzheimer disease (AD) cases is improved in the presence of anxiety symptoms.
Why it matters
In people with mild cognitive impairment, anxiety symptoms were linked to a higher risk of developing Alzheimer's disease over three years. This suggests that watching for anxiety in people with mild cognitive impairment could help identify those more likely to progress.
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Patients with mild cognitive impairment (MCI) showed a high probability to be diagnosed with Alzheimer dementia (AD) after 30 months.
Why it matters
In a community birth cohort followed for 30 months, people with mild cognitive impairment converted to Alzheimer's dementia at high rates, including those with the nonamnestic subtype. This describes how often MCI progresses and does not test any treatment.
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Assessment of Alzheimer's disease (AD)-related neurofibrillary pathology requires a procedure that permits a sufficient differentiation between initial, intermediate, and late stages.
Why it matters
This study describes a method for staging Alzheimer's disease-related neurofibrillary pathology using paraffin sections and immunocytochemistry. It aims to better meet the demands of routine laboratories for assessing the disease process.
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60/100
Smaller hippocampi and specifically CA1 and subicular involvement are associated with increased risk for conversion from MCI to AD.
Why it matters
Researchers at one UCLA centre scanned 20 people with mild cognitive impairment and followed them for 3 years: 6 developed Alzheimer's, 7 stayed the same and 7 improved. On the starting scans, those who developed Alzheimer's had smaller hippocampi on average, 24–27% smaller than those who improved and 9–13% smaller than those who stayed stable, with more shrinkage in the CA1 region; the authors conclude this is "associated with increased risk" of conversion. The groups were very small and no accuracy for predicting any one person's outcome is reported, so this is early group-level evidence, not a test a patient can rely on.
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Atorvastatin therapy may be of benefit in the treatment of mild-to-moderately affected AD patients, but the level of benefit produced may be predicated on earlier treatment, an individual's apolipoprotein E genotype or whether the patient exhibits elevated cholesterol levels.
Why it matters
In this 1-year trial of 67 randomized participants with mild-to-moderate Alzheimer disease, atorvastatin showed a significant positive effect on ADAS-cog performance after 6 months compared with placebo. This effect was more prominent among those entering the trial with higher MMSE scores and cholesterol levels above 200 mg/dl.
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Reality orientation therapy combined with cholinesterase inhibitors has not been evaluated in patients with Alzheimer's disease.
Why it matters
In this randomized trial, 79 of 156 patients taking donepezil for Alzheimer's disease received a reality orientation programme at home for 25 weeks, and the treatment group showed a slight MMSE improvement compared with a decline in controls. This suggests a possible small benefit from combining reality orientation with cholinesterase inhibitors, but it does not indicate a cure or prevention.
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In its earliest clinical phase, Alzheimer's disease characteristically produces a remarkably pure impairment of memory.
Why it matters
This article argues that the earliest clinical phase of Alzheimer's disease mainly affects memory, and that this may begin with subtle changes in how synapses in the hippocampus work, before nerve cells are lost. It suggests the synaptic problems are caused by small, diffusible clumps (oligomers) of amyloid beta protein.
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Starting in 1991, participants were assessed with the Cognitive Abilities Screening Instrument (CASI) and diagnosed with dementia (including subtype) based on published criteria.
Why it matters
In an autopsy sample of 211 Japanese-American men, this study investigated the relationship between cerebral amyloid angiopathy, dementia, and cognitive function. It is a pathology study of associations and does not test any treatment or prevention.
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The results of this preliminary case-control study suggest that estradiol levels may decline significantly in women in whom AD develops.
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To determine the prevalence of early-onset Alzheimer disease (EOAD) and of autosomal dominant forms of EOAD (ADEOAD), we performed a population-based study in the city of Rouen (426,710 residents).
Why it matters
In Rouen (426,710 residents), this 1999 population study found early-onset Alzheimer's disease, defined as onset before age 61, at 41.2 per 100,000 persons at risk, and a strictly defined inherited form (at least three early-onset cases across three generations) at 5.3 per 100,000. In 34 French families with that inherited form, the authors found PSEN1 mutations in 19 (56%), including four variants "not reported elsewhere". These figures describe how common the disease was and which gene was involved in a selected group of families; they are not personal risk estimates, and the study tested no treatment.
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Using parametric methods, no evidence for linkage to the region spanned by the chromosome 12 markers could be detected if familial AD is assumed to arise from the same genetic locus in all 53 families.
Why it matters
In 53 families with multiple members affected by Alzheimer's disease, this study found no evidence for linkage to chromosome 12 markers when assuming all families share the same genetic locus. However, significant evidence for linkage appeared when allowing for locus heterogeneity, supporting the idea that more than one gene may be involved.
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.
- Artificial intelligence in drug development for delirium and Alzheimer’s disease
- Epilepsy and cognitive impairments in Alzheimer disease
- Stem cell-conditioned medium is a promising treatment for Alzheimer's disease
- Randomized Trial of Verubecestat for Mild-to-Moderate Alzheimer's Disease
- Vergleich kinetischer [¹⁸F]PI-2620 Tau-PET Parameter zum longitudinalen Monitoring der Alzheimer-Erkrankung
- Propagation of Tau Pathology in a Model of Early Alzheimer's Disease
- Future directions in Alzheimer's disease from risk factors to prevention
- The role of higher-level cognitive function in gait: executive dysfunction contributes to fall risk in Alzheimer's disease
- Comparative Value of Cognitive and Functional Assessments for Predicting 24-Month Progression from Mild Cognitive Impairment to Alzheimer's Disease: An ADNI Cohort Study
- The impact of congenital heart disease on the timing of Alzheimer's disease in Down syndrome