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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We conclude that PiB-positron emission tomography can detect cerebrovascular beta-amyloid and may serve as a method for identifying the extent of CAA in living subjects.
Why it matters
PiB PET scans detected amyloid in all 6 people with probable cerebral amyloid angiopathy (amyloid deposits in brain blood vessels) and all 9 with probable Alzheimer's. Overall retention was lower in angiopathy than in Alzheimer's but relatively greater in the occipital lobes, and the authors conclude the scan may help gauge angiopathy in living people.
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Baseline MRI scans were characterized by asymmetric T2-hyperintense lesions extending to the subcortical white matter and occasionally the overlying gray matter, with signal properties suggesting vasogenic edema.
Why it matters
This study describes the course of cerebral amyloid angiopathy-related inflammation, including MRI findings, response to immunosuppressive treatment, and a strong link to the APOE epsilon 4/epsilon 4 genotype. It concerns this specific inflammatory condition rather than Alzheimer disease treatment, cure, or prevention.
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53/100
This article discusses how distinct protein aggregates found in various neurodegenerative disorders appear to cause these conditions.
Why it matters
A review of soluble protein oligomers in neurodegeneration, drawing lessons from the Alzheimer's amyloid beta peptide.
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53/100
Low levels of cerebrospinal fluid (CSF) beta-amyloid 1-42 (Abeta42) and high total tau (T-tau) are diagnostic for manifest Alzheimer's disease.
Why it matters
This small longitudinal study of 55 older women examined whether cerebrospinal fluid beta-amyloid 1-42 and total tau measured in 1992 predicted change in Mini-Mental State Examination scores over ten years. It is a biomarker prediction study and does not test any treatment, cure, or prevention.
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The progressive development of Alzheimer disease (AD)-related lesions, such as neurofibrillary tangles (NFT), amyloid deposits and synaptic loss, and the occurrence of microvascular and small macrovascular pathology within the cerebral cortex are conspicuous neuropathologic features of brain aging.
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Magnetic resonance (MR)-based volume measurements of atrophy are potential markers of disease progression in patients with amnestic mild cognitive impairment (MCI) and Alzheimer's disease (AD).
Why it matters
In this longitudinal study, the N-acetylaspartate/creatine ratio declined in people with mild cognitive impairment and Alzheimer's disease compared to cognitively normal elderly, and changes in these metabolite ratios tracked clinical progression about as well as ventricular expansion. This suggests these ratios may be useful markers for tracking how Alzheimer's disease progresses, though the study does not show they can treat or prevent it.
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In some cases, limited nigral pathology suggests extranigral factors in the clinical symptoms of EPS.
Why it matters
This study found that extrapyramidal signs in Alzheimer's disease were associated with substantia nigra pathology including alpha-synuclein aggregation, tau accumulation, and neuron loss. It suggests that this pathology may account for the increasing prevalence of these signs as the disease progresses.
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The authors estimated the effects of each of the three commonly used drugs for Alzheimer disease (donepezil, galantamine, and rivastigmine) in terms of predefined clinical outcomes and trial completion rates, by dosing level, and described differences among them.
Why it matters
This analysis of trials found that donepezil, galantamine, and rivastigmine each improved cognitive test scores compared with placebo, and donepezil and rivastigmine showed larger effects at higher doses. Galantamine and rivastigmine were linked to more people dropping out of trials than placebo, especially at higher doses, so these drugs treat symptoms rather than cure or prevent the disease.
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Higher intake of calories and fats may be associated with higher risk of AD in individuals carrying the apolipoprotein E epsilon4 allele.
Why it matters
In this study of 980 elderly people, those with the highest caloric intake had an increased risk of Alzheimer's disease, and the risk was higher still among people with the apolipoprotein E epsilon4 allele. The association was not statistically significant in people without that allele, so the findings suggest a possible dietary link rather than a proven way to prevent Alzheimer's disease.
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This study suggests that vitamin E from food, but not other antioxidants, may be associated with a reduced risk of AD.
Why it matters
In this community study, higher vitamin E intake from foods was linked to a lower risk of developing Alzheimer's disease, and this link was seen only in people who were APOE epsilon 4 negative. Vitamin C, beta carotene, and vitamin E from supplements were not significantly linked to Alzheimer's risk.
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There were no randomized trials found in the search.
Why it matters
No randomized trials of statins for preventing Alzheimer's disease were found, so there is no good evidence to recommend them for this purpose. The authors note only limited non-randomized evidence that lowering cholesterol might affect the disease process, which is not enough to recommend statins.
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Factor analysis showed four robust and meaningful symptom clusters: factor 1-stereotypic and eating behaviour; factor 2-executive dysfunction and self care; factor 3-mood changes; factor 4-loss of social awareness.
Why it matters
This study examined which neuropsychiatric and behavioural features distinguish frontal and temporal variants of frontotemporal dementia from Alzheimer's disease. It is about differential diagnosis, not about treating, curing or preventing Alzheimer's disease.
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Registration of serial MRI volume images provides a powerful method of quantification of brain atrophy that can be used to monitor progression of AD in clinical trials.
Why it matters
Serial MRI showed that patients with mild to moderate Alzheimer's disease lost brain volume at about 2.37% per year, compared with 0.41% per year in controls, and the authors calculated sample sizes needed to detect a treatment effect. This is a methodological study about measuring progression in trials, not a treatment or cure.
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This study demonstrates that, even in apparently healthy subjects, age-associated immune activation indicated by raised levels of pro-inflammatory cytokines may reflect age-associated pathological processes that develop over decades.
Why it matters
In this group of centenarians, a high blood level of TNF-alpha was linked to both Alzheimer's disease and hardened arteries. This is an association only and does not show that lowering TNF-alpha would treat or prevent dementia.
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Fifteen chromosomal regions warranted initial follow-up.
Why it matters
This genomic screen in families with late-onset Alzheimer disease found the strongest signal on chromosome 12, suggesting a possible new susceptibility gene there. It is a gene-finding study and does not itself provide a treatment, cure or prevention.
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Alzheimer disease is progressive and irreversible, but pharmacologic therapies for cognitive impairment and nonpharmacologic and pharmacologic treatments for the behavioral problems associated with dementia can enhance quality of life.
Why it matters
This consensus statement says Alzheimer disease is progressive and irreversible, but pharmacologic therapies for cognitive impairment and nonpharmacologic and pharmacologic treatments for behavioral problems can enhance quality of life. It does not report any treatment that cures or prevents the disease.
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The relationship between progressive cognitive decline and underlying neuropathology associated with Alzheimer s disease (AD) is a key issue in defining the mechanisms responsible for functional loss.
Why it matters
This study examined the relationship between progressive cognitive decline and underlying neuropathology in Alzheimer's disease, including beta-amyloid deposition, while noting difficulties in comparing such clinical-pathological studies. It is about correlating brain pathology with cognitive status and does not test any treatment, cure or prevention.
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We determined whether a battery of neuropsychological tests could predict who would develop Alzheimer's disease (AD) in a group of 123 memory-impaired nondemented patients.
Why it matters
In 123 people with memory problems but no dementia, followed for 2 years, 29 developed probable Alzheimer's disease. Scores from just two tests at the start, delayed recall on the Rey Auditory Verbal Learning Test and the Wechsler Memory Scale Mental Control subtest, sorted them with 89% accuracy, 76% sensitivity and 94% specificity, so roughly 1 in 4 people who progressed were not flagged. The study predicts who progressed in this one group; it does not show that the tests can rule Alzheimer's in or out for an individual, and it is not about treatment or prevention.
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Apolipoprotein E type 4 allele (apoE epsilon4) is associated with Alzheimer's disease (AD) in the late-onset familial form and in sporadic cases, but the age-associated risk in a randomly sampled elderly population is not established.
Why it matters
In this population-based cohort, people carrying the apolipoprotein E epsilon4 allele had a higher risk of developing Alzheimer's disease, with the highest risk in epsilon4 homozygotes. The study identifies a genetic risk factor only and reports no treatment, cure or prevention.
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In a recent preliminary study it was reported that a severe head injury resulted in the deposition of beta amyloid protein (beta AP) in the cortical ribbon of 30% of patients who survived for less than two weeks.
Why it matters
In this preliminary study, beta amyloid protein deposits were found in one or more cortical areas in 30% of people who died within two and a half years after a severe head injury, and increasing age seemed to increase the extent of these deposits. This suggests that severe head injury can lead to beta amyloid deposition in the brain, but it does not show whether this causes Alzheimer's disease or how to treat, cure, or prevent it.
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Accurate diagnosis of vascular dementia is important for the recognition of underlying pathophysiology and the institution of appropriate therapy.
Why it matters
In 1992 the State of California Alzheimer's Disease Diagnostic and Treatment Centers proposed criteria for diagnosing ischemic vascular dementia, aiming to help tell it apart from Alzheimer's disease, a distinction the authors call "often problematic", and to make counts of how common each condition is more reliable. The criteria use neuroimaging, stress confirmation by brain examination after death, and define "possible" and "mixed" categories that parallel the existing Alzheimer's criteria, so that studies classifying vascular dementia subtypes the same way can be compared and pooled. This is a proposal for how to diagnose, not a test of how accurate the criteria are, and it reports no treatment results.
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53/100
A randomized, double-blind, placebo-controlled, parallel-group clinical trial was carried out to compare 24-week periods of treatment with 1 g acetyl-l-carnitine twice daily and placebo in the treatment of patients with dementia of the Alzheimer type.
Why it matters
In this 24-week trial of 36 patients, acetyl-l-carnitine showed trends toward less deterioration on some memory and reaction-time measures, but no changes reached statistical significance, partly because so few patients completed the study. The results are inconclusive and do not establish acetyl-l-carnitine as an effective treatment.
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We reviewed 81 patients with dementia and autopsy findings of Alzheimer's disease (AD) to identify patients with seizures or myoclonus after onset of dementia.
Why it matters
In a review of 81 patients with autopsy-confirmed Alzheimer's disease, 10% had seizures and another 10% had myoclonus, with seizures occurring at any stage and myoclonus often late. It describes these as manifestations of the illness and offers no treatment, cure or prevention.
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Twenty-one patients with a clinical diagnosis of dementia of the Alzheimer's type (DAT) and 29 healthy, age-matched controls were studied using positron emission tomography (PET) and [18F]2-fluoro-2-deoxy-D-glucose to measure regional cerebral glucose consumption in the resting state.
Why it matters
PET scans showed reduced metabolism in certain brain regions and increased right-left differences even in mild Alzheimer's disease, but these metabolic measures did not change over time in followed patients. This means PET can help show regional brain dysfunction early, but it did not track worsening of the disease in this study.
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Overall, both algorithms demonstrated comparable performance in MA and FFS populations, with high specificity (>97.9%) and negative predictive value [NPV] (>92.9%).
Why it matters
This study evaluated how well two claims-based algorithms identify dementia in Medicare Advantage versus fee-for-service populations. It found high specificity but lower sensitivity in Medicare Advantage in some years, which is about identifying cases for research or planning rather than treating or curing the disease.
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.
- Body fluid cytokine levels in mild cognitive impairment and Alzheimer's disease: a comparative overview
- Three-week nutritional supplementation effect on long-term nutritional status of patients with mild Alzheimer disease
- Errorless learning of a video call in Alzheimer Disease: verbal motor error dissociation as a potential marker of procedural learning (a pilot study)
- Anticorpos anti-amiloide no tratamento da Doença de Alzheimer: uma revisão narrativa
- Mitochondria-associated ER membranes in Alzheimer disease
- The effects of a walking/talking program on communication, ambulation, and functional status in residents with Alzheimer disease
- Alzheimer's disease: Molecular aspects and treatment opportunities using herbal drugs
- Alzheimer CSF biomarkers may be misleading in normal-pressure hydrocephalus
- The economic value of plasma p ‐tau217 testing for patients presenting with cognitive impairment in the United States
- Involvement of Maillard reactions in Alzheimer disease