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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AD is a public health epidemic, which seriously impacts cognition, mood and daily activities; however, one type of activity, exercise, has been shown to alter these states.
Why it matters
This one-year study of early-stage Alzheimer's disease patients found that sedentary patients had significant decline in MMSE scores while active patients, who walked weekly, had less decline in global cognition. It suggests walking may help stabilize cognitive functioning, but it is an observational study and not a test of a cure or prevention.
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The global prevalence of dementia has been estimated to be as high as 24 million, and is predicted to double every 20 years until at least 2040.
Why it matters
This review states that the cause of Alzheimer's disease remains unclear and is likely due to both genetic and environmental factors. It discusses prevalence, incidence, and risk and protective factors but reports no treatment or cure.
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The cognitive functions of the patients in the CMG and WMG were improved after treatment.
Why it matters
Cognitive function improved in both the Chinese medicine and Western medicine groups of patients with mild to moderate Alzheimer disease. The study does not report whether one treatment was better than the other, and it does not show a cure or prevention.
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51/100
Apolipoprotein E (APOE) genotype is the major genetic risk factor for Alzheimer disease (AD); the ε4 allele increases risk and the ε2 allele is protective.
Why it matters
This review describes how apolipoprotein E and its receptors affect Alzheimer's risk, including effects on amyloid-beta aggregation and clearance, synaptic plasticity, lipid transport and inflammation. It discusses possible therapeutic strategies targeting apolipoprotein E or its receptors, but no such treatment is yet established.
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The misfolding and aggregation of specific proteins is a seminal occurrence in a remarkable variety of neurodegenerative disorders.
Why it matters
This review proposes that the formation and spread of protein aggregates in Alzheimer's disease and other neurodegenerative disorders may involve a common mechanism of corruptive protein templating, similar to prion disease. It is a conceptual review, not a treatment trial, so it does not show that any therapy works.
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Alzheimer's disease (AD) is a progressive age-related neurodegenerative disease.
Why it matters
This review discusses neuroimaging measures that may help detect Alzheimer's disease before dementia symptoms appear, when treatment might be more effective. It does not report new treatments or cures, only the potential of imaging biomarkers for early diagnosis.
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Human studies are reviewed concerning whether "aging"-related mechanisms contribute to Alzheimer's disease (AD) pathogenesis.
Why it matters
This review argues that Alzheimer's disease is defined by specific neuropathology driven by genetic factors related to amyloid precursor protein, not by aging itself. It concludes it may be most fruitful to focus on specific pathways involved in Alzheimer's disease rather than attributing it to an inevitable consequence of aging.
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Using a targeted proteomic screen, we identified novel candidate biomarkers that complement the best current CSF biomarkers for distinguishing very mildly/mildly demented from cognitively normal individuals.
Why it matters
This study used a multiplexed immunoassay panel to identify new cerebrospinal fluid biomarkers for Alzheimer's disease diagnosis and prognosis. It found that combinations of markers improved diagnostic performance over the tau/Aβ42 ratio, but it is about diagnosis, not treatment or cure.
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This article introduces a hypometabolic convergence index (HCI) for the assessment of Alzheimer's disease (AD); compares it to other biological, cognitive and clinical measures; and demonstrates its promise to predict clinical decline in mild cognitive impairment (MCI) patients using data from the AD Neuroimaging Initiative (ADNI).
Why it matters
A hypometabolic convergence index derived from FDG-PET differed significantly across probable Alzheimer's, mild cognitive impairment converter, mild cognitive impairment stable and normal groups and correlated with disease severity. Alone or with other biomarkers, it has potential to help characterize Alzheimer's disease and predict clinical decline, but it is not a treatment.
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Behavioural and psychological symptoms of dementia (BPSD) are non-cognitive symptoms commonly associated to Alzheimer's disease (AD).
Why it matters
This cross-sectional study described the clinical profile of people with Alzheimer's disease in Spain and looked at how behavioural and psychological symptoms relate to disease severity. It is observational and aimed at understanding disease evolution and improving diagnosis and treatment, not at testing a cure or prevention.
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51/100
Alzheimer's Disease Neuroimaging Initiative database.
Why it matters
Using spinal-fluid levels of amyloid-beta 1-42, total tau and phosphorylated tau (181P) from the Alzheimer's Disease Neuroimaging Initiative, this study let the measurements sort themselves into patterns without being told who had been diagnosed, then checked the result in 2 further data sets, 1 of them confirmed at autopsy. Its title reports that the Alzheimer-type pattern it found was also present in some cognitively normal older people. The summary held here ends before the results, so no percentages or accuracy figures are available, and as a biomarker study it cannot show that the pattern means a person will develop dementia or that any treatment would prevent it.
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Executive predominant AD may reflect an alternative underlying pathophysiology related to genetic status, reflected in more prominent pathological alterations in frontoparietal regions subserving executive function.
Why it matters
Among people with very mild Alzheimer's dementia, a subgroup with predominant executive problems rather than memory problems had more difficulty with judgement and problem solving and possibly faster progression. The authors say these findings deserve further investigation and may have implications for diagnosis and prognosis, but no treatment was tested.
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Many elderly individuals remain dementia-free throughout their life.
Why it matters
In 299 non-demented elderly people with autopsy, variants in the RELN gene were associated with having many neurofibrillary tangles despite staying dementia-free. The authors suggest reelin may be a compensatory response, but this is a genetic association study and does not test treatment.
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The amyloid hypothesis has yielded a series of well-validated candidate drug targets with potential for the treatment of Alzheimer disease (AD).
Why it matters
This review discusses that alpha-, beta-, and gamma-secretases are potential drug targets for Alzheimer's disease but that inhibiting them may cause mechanism-based toxicity because they have other important biological roles. It summarizes therapeutic potential and challenges but does not report a new treatment.
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Autosomal-dominant Alzheimer's disease has provided significant understanding of the pathophysiology of Alzheimer's disease.
Why it matters
Reviews clinical, pathological, imaging, biochemical and molecular studies of autosomal-dominant (dominantly inherited) Alzheimer's disease and compares it with the more common sporadic form. It presents the Dominantly Inherited Alzheimer Network and its clinical trials initiative, which may test the amyloid hypothesis and the timing of treatment and lead the way to prevention.
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Cerebral amyloid angiopathy is caused by deposition of the amyloid beta protein in the cerebral vasculature.
Why it matters
This study found strongly decreased cerebrospinal fluid amyloid-beta 40 and amyloid-beta 42 in patients with cerebral amyloid angiopathy, a condition caused by amyloid-beta deposition in blood vessels. It is a biomarker observation about a different disease and does not show any treatment, cure, or prevention for Alzheimer disease.
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Clusters of CSF biomarker levels are related to cognitive profiles in Alzheimer disease.
Why it matters
In 177 people who already had Alzheimer's, a spinal-fluid test split them into three groups. The smallest group, 17 people (10%), had very high tau and p-tau, and it did worse on tests of memory, mental speed and executive function. That group did not differ from the others in age, education, APOE genotype, disease duration or overall severity, which suggests that Alzheimer's can look different in different people. This is a one-time snapshot, not a treatment study, and it does not show that tau causes the difference.
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Larger brain and hippocampal volumes were associated with preserved cognitive function during life despite a high burden of Alzheimer disease (AD) pathologic lesions at death.
Why it matters
Among 36 people with high Alzheimer disease pathology at autopsy, those who had normal cognitive function before death had significantly larger antemortem hippocampal and total brain volumes than those diagnosed with Alzheimer disease. This suggests larger brain and hippocampal volumes are associated with preserved cognition despite high pathology, but it does not identify a treatment.
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One of the main features of Alzheimer's disease (AD) is the severe reduction of the cerebral metabolic rate for glucose (CMRglc).
Why it matters
This review describes evidence that reduced cerebral glucose metabolism occurs at preclinical stages of Alzheimer's disease in at-risk groups, and links this to altered energy metabolism and oxidative stress. It reports no treatment, cure or prevention.
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Uptake of carbon 11-labeled Pittsburgh Compound B ([(11)C]PiB) was measured for participants assessed between August 15, 2003, and January 8, 2008, at the Washington University Alzheimer's Disease Research Center and diagnosed either as nondemented (n = 161) or with dementia of the Alzheimer type (n = 37).
Why it matters
In people with elevated brain amyloid measured by carbon 11-labeled Pittsburgh Compound B, more years of education were linked to better cognitive scores, supporting the idea of cognitive reserve. This does not show that education prevents Alzheimer's disease or that it changes the underlying pathology.
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Disruptive behavior is very common in AD and predicts cognitive decline, functional decline, and institutionalization but not mortality.
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51/100
The regions of loss observed in subjects with amnestic mild cognitive impairment (aMCI) who progressed to Alzheimer disease (AD) within 18 months of the MRI are typical of subjects with AD.
Why it matters
People with amnestic mild cognitive impairment who progressed to Alzheimer's disease within 18 months showed gray matter loss in several brain regions, while those who remained stable showed no such loss compared with controls. This helps describe imaging patterns that predict progression but does not provide a treatment or cure.
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These findings suggest that neuropsychiatric symptoms in MCI are a predictor of progression to AD.
Why it matters
In this small study of 51 people with mild cognitive impairment, those who progressed to Alzheimer's disease were more likely to have neuropsychiatric symptoms such as depression and apathy at baseline. The authors suggest these symptoms may help identify people at highest risk, but this does not show that treating the symptoms prevents dementia.
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Beta-amyloid (Abeta) deposition is pathognomic for Alzheimer's disease (AD), but may occur in normal elderly people without apparent cognitive effect.
Why it matters
In 31 people with Alzheimer's disease, 33 with mild cognitive impairment and 32 healthy older adults scanned with PIB PET, increased amyloid binding was found in 97%, 61% and 22% respectively. Amyloid was strongly related to poorer episodic memory in mild cognitive impairment and in healthy older adults, which the authors suggest marks people on the path to Alzheimer's disease.
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Transgenic mice carrying disease-linked forms of genes associated with Alzheimer disease often demonstrate deposition of the beta-amyloid as senile plaques and cerebral amyloid angiopathy.
Why it matters
This study characterized the natural history of amyloid-beta deposition in APPswe/PS1dE9 transgenic mice, showing deposition by 4 months with progressive increases in plaque number and amyloid-beta levels up to 12 months. It is an animal model study and reports no treatment, cure or prevention in humans.
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.
- Microbleeds do not affect rate of cognitive decline in Alzheimer disease
- Preventing Alzheimer's disease-related gray matter atrophy by B-vitamin treatment
- Results from a Phase II Study to Assess the Clinical and Immunological Activity of AFFITOPE® AD02 in Patients with Early Alzheimer's Disease
- Rediscovery of the case described by Alois Alzheimer in 1911: historical, histological and molecular genetic analysis
- Association of Early-Onset Alzheimer Disease With Elevated Low-Density Lipoprotein Cholesterol Levels and Rare Genetic Coding Variants of APOB
- Alzheimer's disease: redox dysregulation as a common denominator for diverse pathogenic mechanisms
- Intra-individual variability in Alzheimer's disease and cognitive aging: definitions, context, and effect sizes
- [The role of CSF markers in the early diagnosis of Alzheimer's disease]
- Cerebrospinal fluid neurogranin and YKL-40 as biomarkers of Alzheimer's disease
- A novel Alzheimer disease locus located near the gene encoding tau protein