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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Infant ε4 carriers had lower MWF and GMV measurements than noncarriers in precuneus, posterior/middle cingulate, lateral temporal, and medial occipitotemporal regions, areas preferentially affected by AD, and greater MWF and GMV measurements in extensive frontal regions and measurements were also significant in the subset of 2- to 6-month-old infants (MWF differences, P Conclusions and relevance While our findings should be considered preliminary, this study demonstrates some of the earliest brain changes associated with the genetic predisposition to AD.
Why it matters
In this cross-sectional imaging study, infants carrying the APOE epsilon 4 allele had differences in white matter myelin water fraction and gray matter volume compared with noncarriers. These are early structural findings in infants and do not show that any treatment or prevention is possible.
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The speed and severity of clinical progression after Alzheimer disease (AD) diagnosis varies and depends on multiple factors, most not well elucidated.
Why it matters
In amnestic mild cognitive impairment, high body mass index was associated with slower progression and weight loss with faster progression, while in Alzheimer's disease no significant differences were seen by BMI or weight change. These findings suggest BMI and weight change may serve as early prognostic indicators, but they do not show that changing weight alters the disease.
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Education, occupation, premorbid intelligence, and brain size are surrogate markers for cognitive reserve.
Why it matters
In this longitudinal study, higher education, occupation, and reading-test scores were linked to a slower decline in one Alzheimer's biomarker in people with normal cognition, and reading scores were linked to slower decline in another biomarker in people with Alzheimer's disease. These markers did not affect the rate of hippocampal shrinkage in any group.
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Clinico-pathological correlation studies and positron emission tomography amyloid imaging studies have shown that some individuals can tolerate substantial amounts of Alzheimer's pathology in their brains without experiencing dementia.
Why it matters
Examining brains after death, this study found that some people who had no dementia during life carried as much amyloid-β plaque and tangle pathology as people with Alzheimer's dementia. Compared with the dementia cases, these "mismatch" brains showed preserved neurons and synapses, less fibrillar and oligomeric amyloid-β deposits, no build-up of abnormal tau at synapses, and much less glial (inflammatory-cell) activation, while soluble amyloid-β levels did not differ significantly. The authors conclude that plaques and tangles "do not inevitably" lead to dementia in everyone; this is a post-mortem association, not a treatment or prevention finding.
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The dynamics of cerebrospinal fluid (CSF) tau and Aβ biomarkers over time in Alzheimer's disease (AD) patients from prodromal pre-symptomatic to severe stages of dementia have not been clearly defined and recent studies, most of which are cross-sectional, present conflicting findings.
Why it matters
This study measured tau and amyloid biomarker levels in spinal fluid over up to 48 months in people with Alzheimer's dementia, mild cognitive impairment, and normal cognition. It describes how these biomarkers change over time, which may inform future research, but it does not test any treatment, cure, or prevention.
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55/100
When patients with MCI underwent clinical follow-up, 29 progressed to dementia, while 44 remained stable.
Why it matters
In 73 patients with mild cognitive impairment followed clinically, incident dementia increased with greater biological severity based on amyloid, metabolism and atrophy biomarkers. The authors conclude the core biomarker pattern is in line with the current pathophysiologic model of Alzheimer's disease.
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Positron emission tomography (PET) of brain amyloid b is a technology that is becoming more available, but its clinical utility in medical practice requires careful definition.
Why it matters
A task force convened by the Alzheimer's Association and the Society of Nuclear Medicine and Molecular Imaging searched the published literature and reached a "consensus of expert opinion" on which patients and clinical situations amyloid PET brain scans could appropriately be used for, and which uses are inappropriate. The authors state that "empirical evidence of impact on clinical outcomes is not yet available", so these are expert criteria and not proof that scanning helps patients. They also say the criteria "will require periodic reassessment" as dementia care and the technology change, so check for a newer version before relying on this 2013 report.
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Greater intracranial volume (ICV) has been associated with less severe Alzheimer's disease (AD) symptoms at a given level of cerebral pathology.
Why it matters
This longitudinal ADNI study of 674 subjects examined whether intracranial volume modifies the link between clinical progression and brain atrophy or apolipoprotein E genotype. It is an observational study, so it cannot show that brain size protects against or treats Alzheimer's disease.
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55/100
Autosomal-dominant Alzheimer disease (ADAD) is a genetic disorder caused by mutations in Amyloid Precursor Protein (APP) or Presenilin (PSEN) genes.
Why it matters
This study compared APP processing in the brain between autosomal-dominant and sporadic Alzheimer's disease and found distinct patterns. It is a brain tissue study and does not report any treatment, cure, or prevention for Alzheimer's disease.
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These results indicate an association between brain hypoperfusion and the dementia of AD.
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Age and APOE genotype are useful predictors of the likelihood of significant amyloid accumulation, but discrimination is modest.
Why it matters
In 483 cognitively normal older adults, age and APOE genotype were the best available predictors of having significant amyloid on PET imaging, though discrimination was only modest. This is about screening to identify people with amyloid, not about treating or preventing Alzheimer's disease.
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The mechanisms by which mutations in the presenilins (PSEN) or the amyloid precursor protein (APP) genes cause familial Alzheimer disease (FAD) are controversial.
Why it matters
This study used kinetic experiments to show that familial Alzheimer's disease mutations affect amyloid-beta generation through several different mechanisms. It helps explain how these mutations cause disease but does not test a treatment or cure.
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Alzheimer's disease (AD) results in cognitive decline and altered network activity, but the mechanisms are unknown.
Why it matters
In a mouse model of Alzheimer's disease, reduced activity of inhibitory parvalbumin cells was linked to network dysfunction and cognitive problems. This was an animal study, so it is not yet known whether targeting these cells would help people with Alzheimer's disease.
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A significant increase in global cortical [(11)C]PIB BP(ND) was found in MCI patients, but no changes were observed in AD patients or controls.
Why it matters
This longitudinal PET study examined changes in three tracers in patients with Alzheimer's disease or mild cognitive impairment and in healthy controls. It found increased amyloid load in mild cognitive impairment patients and progressive metabolic impairment in Alzheimer's disease patients, and concluded that one tracer seemed less useful for examining disease progression.
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Cerebral amyloid angiopathy (CAA) results from deposition of β-amyloid in the media and adventitia of small arteries and capillaries of the leptomeninges and cerebral cortex and is a major cause of lobar intracerebral hemorrhage and cognitive impairment in the elderly.
Why it matters
This review discusses cerebral amyloid angiopathy, which results from beta-amyloid deposition in small arteries and capillaries of the brain and is a major cause of lobar intracerebral hemorrhage and cognitive impairment in the elderly. Advanced CAA is present in approximately one-quarter of brains with Alzheimer's disease, but fewer than half of CAA cases meet pathologic criteria for Alzheimer's disease.
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Both low and high body mass index (BMI) has been associated with cognitive impairment and dementia risk, including Alzheimer disease (AD).
Why it matters
This cross-sectional study examined the relationship between body mass index and Alzheimer disease biomarkers measured by PET imaging or cerebrospinal fluid analysis. It describes an association and does not test any treatment, cure, or prevention.
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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that results in progressive loss of bulbar and limb function.
Why it matters
This review covers amyotrophic lateral sclerosis, a neurodegenerative disease with progressive loss of bulbar and limb function, noting that riluzole remains the only effective drug and extends average survival by 3-6 months. It concerns amyotrophic lateral sclerosis diagnosis and management, not Alzheimer's disease treatment, cure or prevention.
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Despite numerous studies on the role of medial temporal lobe structures in Alzheimer's disease (AD), the magnitude and clinical significance of amygdala atrophy have been relatively sparsely investigated.
Why it matters
This imaging study compared amygdala atrophy with hippocampus atrophy in very mild and mild Alzheimer's disease and examined whether amygdala atrophy relates to cognitive and neuropsychiatric status. It is an observational study of brain structure and symptom severity, not a treatment, cure, or prevention study.
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55/100
Co-morbid dementia occurs in approximately 14% of patients with a new diagnosis of ALS.
Why it matters
In 160 newly diagnosed Irish ALS patients compared with 110 matched controls, about 14% met criteria for frontotemporal dementia. The authors report that cognitive impairment, mostly but "not exclusively" in executive (planning and organising) skills, was present in "more than 40%" of those without dementia, while almost half (46.9%) showed no cognitive abnormality. This is an ALS and frontotemporal dementia study, not an Alzheimer's study. It counts how often thinking problems occur at diagnosis and does not test any treatment or prevention.
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The Alzheimer's Association Research Roundtable convened a working group to review data on amyloid imaging related abnormalities (ARIA) in response to concerns raised by the Food and Drug Administration.
Why it matters
Gives recommendations from an Alzheimer's Association Research Roundtable workgroup on amyloid-related imaging abnormalities in trials of amyloid-modifying therapies.
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VRF increased the risk of incident AD dementia.
Why it matters
In 837 people with mild cognitive impairment followed yearly for 5 years, 298 developed Alzheimer's dementia. Those with high blood pressure, diabetes, cerebrovascular disease or high cholesterol were more likely to convert. People whose vascular risk factors were all treated had lower dementia risk than those with only some treated, and treating hypertension, diabetes or high cholesterol was each "associated with the reduced risk of AD conversion." The authors stress that their findings "are observational", so this shows a link, not proof that treatment prevents Alzheimer's.
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Sporadic tauopathies are characterized by differential cellular and topographical predominance of phospho-tau immunoreactivity and biochemical distinction of the tau protein.
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This article focuses on the effects of operational differences in case ascertainment on estimates of prevalence and incidence of cognitive impairment and/or dementia of the Alzheimer type.
Why it matters
This article discusses how differences in diagnostic criteria affect estimates of Alzheimer's disease prevalence and incidence. It does not test a treatment, cure, or prevention, and it highlights that how cases are defined strongly influences numbers.
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High HDL-C levels in elderly individuals may be associated with a decreased risk of AD.
Why it matters
In this cohort of elderly people without cognitive impairment at baseline, higher HDL cholesterol levels were associated with a decreased risk of Alzheimer disease. This is an observed association and does not show that raising HDL cholesterol would prevent Alzheimer's.
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Clinicopathologic studies of Parkinson disease dementia (PDD) and dementia with Lewy bodies (DLB) commonly reveal abnormal β-amyloid deposition in addition to diffuse Lewy bodies (α-synuclein aggregates), but the relationship among these neuropathologic features and the development of dementia in these disorders remains uncertain.
Why it matters
This study found that amyloid imaging with Pittsburgh Compound B did not distinguish between different Lewy body-associated disorders, and elevated amyloid binding was not associated with earlier onset or faster progression of cognitive impairment. The findings suggest that fibrillar amyloid-β does not distinguish these disorders and do not support amyloid imaging as a way to track or treat them.
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.
- Automated mapping of hippocampal atrophy in 1-year repeat MRI data from 490 subjects with Alzheimer's disease, mild cognitive impairment, and elderly controls
- Both total and phosphorylated tau are increased in Alzheimer's disease
- Longitudinal Clinical and Cognitive Changes Along the Alzheimer Disease Continuum in Down Syndrome
- New advances in NMDA receptor pharmacology
- Mitochondria-associated ER membranes and Alzheimer disease
- An inventory to assess activities of daily living for clinical trials in Alzheimer's disease. The Alzheimer's Disease Cooperative Study
- Imaging cerebral atrophy: normal ageing to Alzheimer's disease
- The Gut Microbiota as a Mediator Linking the MIND Diet to Alzheimer’s Disease
- Plasma phospho‐tau181 increases with Alzheimer's disease clinical severity and is associated with tau‐ and amyloid‐positron emission tomography
- Antihypertensive medications and risk for incident dementia and Alzheimer's disease: a meta-analysis of individual participant data from prospective cohort studies