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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53/100
Discovery efforts for susceptibility loci for Alzheimer disease could benefit from the use of neuropathologic intermediate phenotypes as a complement to other approaches.
Why it matters
This study found that using measures of Alzheimer brain pathology strengthened the genetic association with APOE, and that APOE epsilon2 was linked to Alzheimer pathology even though it was not linked to clinical Alzheimer disease. It is about improving genetic research methods, not about treating or preventing the disease.
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Vascular dysfunction has a critical role in Alzheimer's disease (AD).
Why it matters
This review describes evidence that cerebrovascular dysfunction, including cerebral hypoperfusion and impaired amyloid-beta clearance across the blood-brain barrier, may precede cognitive decline and contribute to the onset and progression of Alzheimer's disease. It proposes mechanisms for future investigation but reports no treatment, cure or prevention.
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The MAPT Study is the first preventive trial involving multidomain interventions.
Why it matters
This paper describes the design of an ongoing 3-year trial in 1,200 frail elderly people testing whether a multidomain intervention (nutrition, physical activity, and cognitive training) plus omega-3 treatment can prevent cognitive decline. No results are reported yet, so it is too early to know whether these approaches are effective.
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53/100
In recent years a rapidly increasing number of studies has focused on the relationship between dementia and metabolic disorders such as diabetes, obesity, hypertension, and dyslipidemia.
Why it matters
This review discusses relationships between dementia and metabolic disorders such as diabetes, obesity, hypertension and dyslipidemia, and highlights convergent mechanisms such as insulin resistance that may increase dementia risk. It reports no treatment, cure or prevention, only proposed directions for future strategies.
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Semiautomated, individually specific quantitative MR imaging methods can be used to identify a pattern of regional atrophy in MCI that is predictive of clinical decline.
Why it matters
A pattern of brain atrophy measured on MRI distinguished people with mild Alzheimer's disease from healthy controls with 83% sensitivity and 93% specificity. People with mild cognitive impairment who had this atrophy pattern showed greater one-year decline and were more likely to progress to probable Alzheimer's disease (29% per year versus 8%).
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53/100
More than 25 million people in the world today are affected by dementia, most suffering from Alzheimer's disease.
Why it matters
This review points to vascular risk factors as potential risks for Alzheimer's disease and suggests that psychosocial factors like physical exercise and mentally stimulating activity may be beneficial. It proposes that long-term multidomain interventions could reduce or postpone dementia, but this is a hypothesis not yet proven by the review.
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Medial temporal lobe atrophy (MTA) scores 1) distinguish probable Alzheimer disease (AD) and amnestic mild cognitive impairment (MCI) subjects from nonamnestic MCI and no cognitive impairment (NCI) subjects, 2) help predict diagnosis at baseline, and 3) predict transition from NCI to MCI and from MCI to probable AD.
Why it matters
Medial temporal lobe atrophy scores distinguished probable Alzheimer disease and amnestic mild cognitive impairment from other groups with 85%/82% and 80%/82% sensitivity/specificity, and predicted diagnostic transitions at one year. This is a diagnostic aid only, not a treatment or cure.
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53/100
This report of 25(OH)D concentrations in a predominantly white PD cohort demonstrates a significantly higher prevalence of hypovitaminosis in PD vs both healthy controls and patients with AD.
Why it matters
This study measured vitamin D in stored blood samples from one US research database. Parkinson patients were compared with Alzheimer patients (n = 97) and healthy controls (n = 99), matched for age, sex, race, APOE genotype and location. More Parkinson patients had insufficient vitamin D (55%) than Alzheimer patients (41%) or controls (36%), and their average level was the lowest (31.9 vs 34.8 and 37.0 ng/mL). For Alzheimer's readers, the study's main point is about Parkinson's; it is a one-time comparison in a mostly white group and does not show that vitamin D changes the risk or course of either disease.
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The mean whole-brain atrophy rate was -1.9 +/- 0.9% per year.
Why it matters
In this group of Alzheimer patients, younger age, absence of APOE epsilon4, and lower MMSE scores were linked to faster whole-brain shrinkage over about 1.7 years. This describes which patients may lose brain volume faster and does not report a treatment.
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The objective of this study was to analyze factors influencing the risk and timing of Alzheimer's disease (AD) in central Norway.
Why it matters
This case-control study from central Norway found that the APOE epsilon4 allele is a risk factor for late-onset Alzheimer's disease and lowers the age at onset. It identifies a risk factor only and reports no treatment, cure or prevention.
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These data suggest that having both diabetes and APOE epsilon4 increases the risk of dementia, especially for AD and mixed AD.
Why it matters
This prospective study found that people with both type 2 diabetes and the APOE epsilon 4 allele had a significantly higher risk of Alzheimer disease and mixed dementia. It identifies a combined risk factor but does not test any treatment, cure, or prevention.
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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.
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.
- 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
- Patients with Alzheimer disease have lower levels of serum anti-amyloid peptide antibodies than healthy elderly individuals
- Anosognosia in Alzheimer disease: Disconnection between memory and self-related brain networks
- AD-HOLDER: Alzheimer’s Disease Detection via Machine Learning based Histograms of Light GBM Classifier using MRI and PET Images