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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In a recent crossover trial, methylphenidate treatment decreased apathy in Alzheimer's disease.
Why it matters
This six-week randomized, double-blind, placebo-controlled trial assessed methylphenidate 20 mg daily versus placebo for apathy in people with Alzheimer's disease. It is about treating apathy as a symptom and does not show any effect on curing or preventing Alzheimer's disease.
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Sleep and circadian problems are very common in Alzheimer disease (AD).
Why it matters
Sleep and circadian problems are "very common in Alzheimer disease," and the authors note that "recent animal studies suggest a bidirectional relationship between sleep and β-amyloid." This cross-sectional study of community volunteers at the Washington University Knight Alzheimer's Disease Research Center (October 2010 to June 2012) asked whether amyloid build-up in people who do not yet have memory or thinking problems goes along with changes in how well or how long they sleep. Our stored summary ends before the results, so check the original paper for what it found; a single snapshot like this can show an association but not which came first, and it tests no treatment.
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In subjects with MCI and evidence of amyloid pathology, the injury markers CSF t-tau and p-tau and hippocampal atrophy can predict further cognitive decline.
Why it matters
In 110 subjects with mild cognitive impairment and abnormal CSF amyloid, 57% progressed to Alzheimer's-type dementia over a mean of 2.2 years, and abnormal CSF tau and hippocampal atrophy predicted faster progression. These markers may help identify those at higher risk, but no treatment is tested.
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67/100
Twenty-seven (27.3%) of the 99 women developed incident dementia.
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67/100
Florbetapir F 18 PET can image amyloid-β (Aβ) aggregates in the brains of living subjects.
Why it matters
In 151 people, including those with mild cognitive impairment, normal cognition and Alzheimer's dementia, florbetapir PET was used to detect amyloid-beta and assess later cognitive decline over 18 months. This is a prognostic imaging study and does not show any treatment, cure or prevention.
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However, few longitudinal Pittsburgh compound B-positron emission tomography studies have tested this hypothesis, and with conflicting results.
Why it matters
In this longitudinal PET imaging study, only Pittsburgh compound B status had a significant effect: both positive and negative subjects showed increasing amyloid-β deposition, with a greater increase in those who were positive. Clinical status and disease progression did not show a significant effect on the rate of amyloid-β accumulation.
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67/100
The APOE-ε4 allele is associated with a moderately increased risk for progression from MCI to AD-type dementia.
Why it matters
This meta-analysis of 35 studies found that carrying the APOE-ε4 allele is associated with a moderately increased risk of progressing from mild cognitive impairment to Alzheimer's-type dementia, with an odds ratio of 2.29. However, the sensitivity and specificity were modest, so the allele alone is not a precise predictor.
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Summary results for patients with mild AD were obtained by contrasting the summary results for patients with mild or moderate AD with the summary results for the subset of patients with moderate AD.
Why it matters
This analysis found no significant differences between memantine and placebo on any outcome for patients with mild Alzheimer's disease, either within any trial or when data were combined. The authors report a lack of evidence for memantine's efficacy in mild Alzheimer's disease.
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Florbetapir-PET imaging was performed a mean of 99 days (range, 1-377 days) before death for the 29 individuals in the primary analysis cohort.
Why it matters
In 29 people from hospice, long-term care and community settings who had a florbetapir amyloid PET scan a mean of 99 days before death, both how doctors read the scans and the measured uptake were correlated with the amount of β-amyloid found in their brains at autopsy (ρ 0.78, 95% CI 0.58–0.89). The authors say this is evidence that a scan can identify amyloid in the living brain. They also say more studies were needed to know how the scan should be used to diagnose Alzheimer's or to predict who will develop dementia.
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Numerous studies have reported a smaller hippocampal volume in Alzheimer's disease (AD) patients than in aging controls.
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The CSF AD profile was more common in patients with SCI (31 of 60 [52%]), naMCI (25 of 37 [68%]), and aMCI (56 of 71 [79%]) than in healthy controls (28 of 89 [31%]).
Why it matters
A spinal fluid profile indicating Alzheimer's-type changes was common in people with subjective or mild cognitive impairment and was linked to later cognitive decline. This supports using such markers to identify who may decline, but it does not provide a treatment or cure.
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Ibuprofen, if used for relatively short periods of time and although well tolerated thanks to gastroprotection, does not seem to be effective in tertiary prevention of mild-moderate AD.
Why it matters
In this 12-month randomized, double-blind, placebo-controlled trial, ibuprofen did not slow cognitive progression in mild to moderate Alzheimer's disease, with similar ADAS-Cog worsening in both groups and no differences in secondary outcomes. The authors concluded ibuprofen does not seem effective in tertiary prevention of mild-moderate Alzheimer's disease.
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67/100
CSF A beta(1-42) was the most sensitive biomarker for AD in the autopsy cohort of CSF samples: receiver operating characteristic area under the curve of 0.913 and sensitivity for AD detection of 96.4%.
Why it matters
In an autopsy cohort, cerebrospinal fluid amyloid-beta 1-42 was the most sensitive biomarker for Alzheimer's disease, with 96.4% sensitivity for detection. In the ADNI cohort, an Alzheimer's-like baseline cerebrospinal fluid profile was detected in 33 of 37 mild cognitive impairment subjects who converted to probable Alzheimer's disease during the first year, suggesting the signature may predict conversion.
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This study failed to find a beneficial effect of exogenous melatonin, consistent with a number of other studies.
Why it matters
In this small trial, melatonin had no significant effect on sleep, circadian rhythms, or agitation in institutionalized patients with Alzheimer disease. This means melatonin did not help these symptoms in this study.
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Thinning in specific cortical areas known to be affected by Alzheimer disease (AD) is detectable in individuals with questionable AD dementia (QAD) and predicts conversion to mild AD dementia.
Why it matters
Among people with mild impairment, those who progressed to mild Alzheimer's dementia about 2.5 years later showed greater thinning in temporal and parietal brain regions than those who remained stable. An aggregate measure of these regions predicted progression with 83% sensitivity, but this is about prediction, not treatment or cure.
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OSA may aggravate cognitive dysfunction in dementia and thus may be a reversible cause of cognitive loss in patients with AD.
Why it matters
In this randomized trial of 52 people with mild to moderate Alzheimer's disease and obstructive sleep apnea, comparing 3 weeks of therapeutic versus placebo CPAP showed no significant improvements in cognition, though pre- and post-treatment scores after 3 weeks of therapeutic CPAP in both groups did improve. The study was underpowered to make definitive statements, and it does not show that treating sleep apnea cures or prevents Alzheimer's disease.
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67/100
Senile plaques accumulate over the course of decades in the brains of patients with Alzheimer's disease.
Why it matters
In a mouse model of Alzheimer's disease, this study investigated the timing between amyloid-beta plaque formation and neuronal abnormalities, including the uncertain role of microglia. These are animal findings on plaque development and do not establish a treatment, cure or prevention for Alzheimer's disease in people.
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Atrial fibrillation, hypertension, and angina were associated with a greater rate of decline and may represent modifiable risk factors for secondary prevention in Alzheimer disease.
Why it matters
In people already diagnosed with Alzheimer's disease, atrial fibrillation, systolic hypertension, and angina were linked to faster decline, while bypass surgery, diabetes, and antihypertensive medications were linked to slower decline. This concerns progression after diagnosis, not prevention or cure.
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The NTB had high test-retest reliability at 6 (Pearson product moment correlation [r] = 0.92) and 12 (r = 0.88) months.
Why it matters
This study reports on the psychometric properties of a neuropsychological test battery for measuring drug efficacy in Alzheimer's disease clinical trials. It is about a measurement tool, not a treatment, cure, or prevention for the disease.
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We re-assessed after longer follow-up time in the large population-based cohort of the Rotterdam Study whether smoking habits and pack-years of smoking are associated with the risk of dementia, Alzheimer disease (AD), and vascular dementia (VaD).
Why it matters
This study re-assessed whether smoking habits and pack-years of smoking are associated with the risk of dementia, Alzheimer's disease, and vascular dementia in a large population-based cohort. It is an observational study of a possible risk factor and does not test any treatment, cure, or prevention.
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This study examined the efficacy and safety of memantine monotherapy in patients with moderate-to-severe Alzheimer disease (AD).
Why it matters
In this 24-week, double-blind trial of 350 people with moderate-to-severe Alzheimer's who were not taking a cholinesterase inhibitor, memantine alone (20 mg/day) did not beat placebo on the planned main test of thinking (the SIB) at week 24. It did show an advantage at weeks 12 and 18, and again at week 24 when the researchers used a different statistical method. Daily-living ability "did not differ significantly between groups in any analysis," and side effects were similar with memantine and placebo, so the result is mixed rather than a clear win.
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The very mildest symptomatic stage of AD exhibits the same CSF biomarker phenotype as more advanced AD.
Why it matters
In 139 research volunteers aged 60–91, people with very mild or mild Alzheimer's had lower spinal-fluid Aβ42 and higher tau and phosphorylated tau than people without dementia, and spinal-fluid Aβ42 "completely corresponds" with amyloid seen on PET scans. Among those who were cognitively normal at the start, higher tau/Aβ42 and p-tau181/Aβ42 ratios predicted moving to the first stage of clinical impairment over 1–8 years (adjusted hazard ratios 5.21 and 4.39, with wide 95% intervals of 1.58–17.22 and 1.62–11.86). This is an observational prediction study: it shows an association, gives no cut-off for individual testing, and does not test any treatment or prevention.
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High concentrations of Abeta(1-40) but not Abeta(1-42) at baseline were associated with an increased risk of dementia.
Why it matters
This cohort study found that high plasma Abeta(1-40) concentrations were associated with increased dementia risk, while a higher Abeta(1-42)/Abeta(1-40) ratio was associated with reduced risk. It identifies a possible blood marker of risk but does not test any treatment, cure, or prevention.
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Estrogen replacement therapy for 1 year did not slow disease progression nor did it improve global, cognitive, or functional outcomes in women with mild to moderate AD.
Why it matters
In this trial of 120 women with mild to moderate Alzheimer disease, estrogen replacement therapy did not significantly differ from placebo on the primary global measure, and 80% of those taking estrogen worsened compared with 74% taking placebo. Secondary measures also showed no significant differences, except the Clinical Dementia Rating Scale, which suggested worsening among patients taking estrogen.
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One hundred eighty-seven participants with brain autopsy (NPDx1: AD n = 85; other n = 102; mean age: 74.3 years, 38.5% female; interval blood collection-death [mean ± SD]: 2.8 ± 1.6 years) and 67 NC without brain autopsy (mean age: 66.5 years, 71.6% female) were included. pTau217, but not GFAP, levels increased stepwise with increasing Thal phases (β = 0.61; 95% CI [0.24-0.97] to β = 0.91 [0.55-1.27]) and Braak stages (β = 0.59; [0.16-1.01] to β = 0.74 [0.33-1.15]).
Why it matters
In this autopsy cohort, plasma pTau217 reflected Alzheimer disease brain pathology even in people with other dementia diagnoses, while GFAP and NfL did not specifically track it. This supports pTau217 as a diagnostic marker, but it does not address treating, curing or preventing 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.
- Soluble Amyloid β Peptide Concentration as a Predictor of Synaptic Change in Alzheimer's Disease
- Characterizing Alzheimer's disease using a hypometabolic convergence index
- Alzheimer Detection And Classification Using SVM
- Alzheimer's disease cerebrospinal fluid biomarkers differentiate patients with Creutzfeldt-Jakob disease and autoimmune encephalitis
- Ethnic differences in beliefs regarding Alzheimer disease among dementia family caregivers
- Diagnostic accuracy of the MMSE in detecting probable and possible Alzheimer's disease in ethnically diverse highly educated individuals: an analysis of the NACC database
- Artificial Intelligence–Based Detection of ARIA on MRI During Alzheimer Disease Therapy: Expert Opinion on Responsible Clinical Integration
- Recommendations for the use of PET imaging biomarkers in the diagnosis of neurodegenerative conditions associated with dementia: SEMNIM and SEN consensus
- Decreased Prevalence of Alzheimer Disease Associated With 3-Hydroxy-3-Methyglutaryl Coenzyme A Reductase Inhibitors
- Biological subtypes of Alzheimer disease: A systematic review and meta-analysis