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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These results are approximately 10 times those usually observed with both nonpharmacological and pharmacological treatments and indicate substantial benefits with the management program for advanced AD persons.
Why it matters
In a 28-week randomized trial of only 20 community-residing people with Alzheimer disease, an individualized person-centered management program added to memantine treatment showed significant benefits on global and daily-living measures. The authors report these benefits were about 10 times those usually seen with treatments, but the very small sample limits how much can be concluded.
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51/100
To better understand how sleep/wake dysregulation affects Alzheimer's disease (AD), we compared the cerebrospinal fluid (CSF) orexin and histamine/tele-methylhistamine (HA/t-MHA) levels of 82 patients (41 probable-AD-high level of evidence, 41 mild cognitive impairment MCI-due-to-AD), 24 other neurologic disorders (OND) and 24 controls.
Why it matters
This study compared CSF orexin-A and histamine levels and sleep profiles among patients with probable Alzheimer's disease, mild cognitive impairment, other neurologic disorders, and controls. It is an observational biomarker and sleep study and does not test any treatment, cure, or prevention.
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This paper presents a brain T1-weighted structural magnetic resonance imaging (MRI) biomarker that combines several individual MRI biomarkers (cortical thickness measurements, volumetric measurements, hippocampal shape, and hippocampal texture).
Why it matters
This paper combines several MRI-based measures to help tell apart mild cognitive impairment and Alzheimer's disease. It is a diagnostic method and does not test any treatment, cure, or prevention.
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This article presents recommendations, based on the Grading of Recommendations, Assessment, Development, and Evaluation method, for the clinical application of cerebrospinal fluid (CSF) amyloid-β 1-42 , tau, and phosphorylated tau in the diagnostic evaluation of patients with mild cognitive impairment (MCI).
Why it matters
These consensus recommendations support using CSF amyloid-β 1-42, tau and phosphorylated tau in the diagnostic workup of mild cognitive impairment to predict decline or conversion to Alzheimer's dementia and guide management. They address diagnosis and prognosis only, not treating, curing or preventing the disease.
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Amyloidosis in the absence of neurodegeneration did not have an adverse impact on practice effects or the 30-month cognitive trajectories.
Why it matters
In cognitively normal older adults, having amyloid buildup alone did not harm thinking over 30 months, but having signs of neurodegeneration was linked to worse thinking later. This suggests that treatments aimed at nerve damage may matter more than targeting amyloid alone in people without symptoms.
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There is a close, but not obligatory, association between logopenic PPA and AD.
Why it matters
This study found a close but not obligatory association between logopenic primary progressive aphasia and Alzheimer's disease neuropathology, and that no language measure could reliably confirm or exclude Alzheimer's disease in these patients. It supports the idea that Alzheimer's disease has biological subtypes and that biomarkers are needed for diagnosis, but it does not test a treatment, cure, or prevention.
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With the advent of genome-wide association studies (GWAS) and next-generation sequencing, more than 20 risk loci that affect Alzheimer's disease have been identified.
Why it matters
This review reports that over 20 risk loci for Alzheimer's disease have been identified, with APOE ɛ4 having a strong effect and the rare TREM2 p.Arg47His variant a lesser one. It is a summary of genetic findings and does not offer a treatment, cure or prevention.
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Suspected non-Alzheimer disease pathophysiology (SNAP) is a biomarker-based concept that applies to individuals with normal levels of amyloid-β biomarkers in the brain, but in whom biomarkers of neurodegeneration are abnormal.
Why it matters
This article describes suspected non-Alzheimer disease pathophysiology (SNAP), a biomarker pattern of normal amyloid-beta but abnormal neurodegeneration markers, present in about 23% of clinically normal people over 65 and about 25% of those with mild cognitive impairment. It is a conceptual and controversial biomarker category, not a treatment, cure, or prevention.
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The new diagnostic criteria for Alzheimer's disease (AD) acknowledges the interest given to biomarkers to improve the specificity in subjects with dementia and to facilitate an early diagnosis of the pathophysiological process of AD in the prodromal or pre-dementia stage.
Why it matters
This consensus statement from the Spanish Society of Nuclear Medicine and Spanish Society of Neurology reviews the evidence on FDG-PET, which measures brain glucose use, and amyloid-PET, which detects amyloid plaques. Based on a systematic literature review, it sets out agreed recommendations on when these scans should be used to diagnose Alzheimer's disease and related dementias. The aim is to help clinicians apply newer diagnostic criteria and catch the disease earlier, including before dementia appears.
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51/100
None of the participants were diabetics, smokers, or met criteria for obesity.
Why it matters
In 52 cognitively normal adults, this cross-sectional study linked certain nutrient patterns to brain markers of Alzheimer's disease, including a pattern of vitamin B12 and D associated with brain measures. Because it is a small cross-sectional study, it cannot show that any nutrient prevents or causes Alzheimer's disease.
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Although typical forms of Alzheimer disease (AD) and Creutzfeldt-Jakob disease (CJD) are clinically distinguishable, atypical AD phenotypes may pose a diagnostic challenge.
Why it matters
This study examined whether cerebrospinal fluid prion protein levels could help tell apart atypical Alzheimer's disease from Creutzfeldt-Jakob disease. It is a diagnostic study and does not offer a treatment, cure, or prevention for Alzheimer's disease.
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Being overweight or obese, as measured with body-mass index or central adiposity (waist circumference), and the trajectory of body-mass index over the life course have been associated with brain atrophy, white matter changes, disturbances of blood-brain barrier integrity, and risk of all-cause late-onset dementia and Alzheimer's disease.
Why it matters
This paper discusses whether hormones released by fat tissue could link obesity to dementia risk. It is a discussion of possible mechanisms and does not test any treatment, cure or prevention.
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Retinal nerve fiber layer thickness (RNFL) measured by means of Optical Coherence Tomography (OCT) has been used as a marker not only of ophthalmologic diseases but also of neurodegenerative diseases such as Alzheimer's disease (AD) and mild cognitive impairment (MCI).
Why it matters
In this cross-sectional study of 18 people with Alzheimer's disease, 21 with mild cognitive impairment, and 41 controls, retinal nerve fiber layer thickness was thinner in mild cognitive impairment than controls and thinner still in Alzheimer's disease. The authors suggest optical coherence tomography could be a useful marker for early detection, not a treatment or cure.
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Recently, ~16% of participants in an anti-Aβ passive immunotherapy trial for mild-to-moderate Alzheimer disease (AD) had a negative baseline amyloid positron emission tomography (PET) scan.
Why it matters
In an autopsy database, about 14% of people clinically diagnosed with mild-to-moderate probable Alzheimer's disease had no or sparse neuritic plaques, which would likely mean a negative amyloid PET scan. The authors conclude that a positive amyloid biomarker should be required for future anti-amyloid drug trials, so this is about trial design rather than a treatment, cure, or prevention.
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The most common and distinctive feature for all pathologies associated with primary progressive aphasia was the asymmetric prominence of atrophy, neuronal loss, and disease-specific proteinopathy in the language-dominant (mostly left) hemisphere.
Why it matters
Across all the pathologies linked to primary progressive aphasia, this study found that the most common and distinctive feature was shrinkage, nerve-cell loss and disease-specific protein build-up concentrated on the language-dominant (mostly left) side of the brain. It also reported that the logopenic form was linked to Alzheimer's disease pathology "much more modest[ly]" than amyloid brain-scan studies had implied. That is a reason to be careful with how such scan results are interpreted; the study does not address treatment.
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Revised diagnostic criteria for Alzheimer disease (AD) acknowledge a key role of imaging biomarkers for early diagnosis.
Why it matters
This analysis found that how an imaging marker is measured can matter as much as which marker is used when separating Alzheimer disease from healthy aging or predicting progression from mild cognitive impairment. It is about improving diagnostic and prognostic accuracy, not about treating, curing, or preventing the disease.
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51/100
Amyloid imaging is currently introduced to the market for clinical use.
Why it matters
This review states that available amyloid PET ligands are valid biomarkers for Alzheimer-related amyloidosis and proposes when amyloid imaging may be useful in a memory clinic. It identifies gaps in evidence on the added value of amyloid imaging in clinical practice and does not test any treatment, cure or prevention.
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Alzheimer's disease (AD) is hallmarked by amyloid plaques, neurofibrillary tangles, and widespread cortical neuronal loss (Selkoe, 2001).
Why it matters
This study developed a transgenic rat model that shows plaques, tau pathology, behavioral impairment, and neuronal loss. It is a new animal model for studying Alzheimer's disease, not a treatment or cure.
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These findings support the idea that vascular amyloid burden directly contributes to chronic cerebral ischemia and highlights the possible utility of amyloid imaging as a marker of CAA severity.
Why it matters
In people with cerebral amyloid angiopathy, amyloid burden on PET correlated with the extent of white matter hyperintensities, but this was not seen in Alzheimer disease or healthy elderly. This supports a link between vascular amyloid and chronic brain ischemia and suggests amyloid imaging may mark disease severity, but it is not a treatment.
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The National Institute on Aging and the Alzheimer’s Association charged a workgroup with the task of developing criteria for the symptomatic predementia phase of Alzheimer’s disease (AD), referred to in this article as mild cognitive impairment due to AD.
Why it matters
This workgroup developed two sets of criteria for mild cognitive impairment due to Alzheimer's disease: core clinical criteria for healthcare providers without advanced imaging or cerebrospinal fluid analysis, and research criteria incorporating biomarkers. The final criteria have four levels of certainty depending on biomarker findings, and considerable work is needed to validate and standardize biomarker analysis for community settings.
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The Alzheimer's Disease Assessment Scale cognitive subscale (ADAS-Cog) is widely used in AD, but may be less responsive to change when used in people with mild cognitive impairment (MCI).
Why it matters
This study added executive functioning and functional ability items to the ADAS-Cog to try to improve its ability to detect change in people with mild cognitive impairment. It is about improving a cognitive test used in trials, not about treating, curing, or preventing Alzheimer's disease.
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51/100
A growing body of evidence demonstrates an association between vascular risk factors and Alzheimer's disease.
Why it matters
In 1,000 autopsy cases, this study found that cerebrovascular atherosclerosis in the circle of Willis correlates with Alzheimer pathology, with more than 77% of Alzheimer's disease subjects showing atherosclerotic plaques. It describes an association between vascular disease and Alzheimer pathology and offers no treatment, cure or prevention.
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Predicting Alzheimer's disease (AD) in individuals with some symptoms of cognitive decline may have great influence on treatment choice and disease progression.
Why it matters
In people with mild cognitive impairment from the ADNI cohort, patterns of cortical thinning on MRI predicted who would later meet criteria for probable Alzheimer's disease with 70% accuracy 3 years beforehand, rising to 76% at 6 months. The authors also showed that letting test subjects into the model-building step "artificially inflated" accuracy to 73–81%, a caution for judging other MRI prediction studies. It is a research prediction method, not a clinical test or a treatment.
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Family history is the second strongest risk factor for Alzheimer disease (AD) following advanced age.
Why it matters
This 2012 review reports that, according to twin and family studies, genes play a role in at least 80% of Alzheimer's cases, and that family history is the strongest risk factor after age. Only rare mutations in APP, PSEN1 and PSEN2 "virtually guarantee" the disease, and they account for about 5% of cases, all early-onset (before 60), while common APOE variants influence susceptibility in about half of late-onset cases. Together these four genes explain only 30–50% of the inherited risk, and the review's count of further candidate genes reflects research as of 2012.
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Alzheimer's disease (AD) can be classified based on the relative density of neurofibrillary tangles (NFTs) in the hippocampus and association cortices into three subtypes: typical AD, hippocampal-sparing AD (HpSp AD), and limbic-predominant AD (LP AD).
Why it matters
This brain-tissue study found that a dementia with tangles mostly in limbic areas differs from limbic-predominant Alzheimer's in age of onset, disease duration and tangle stage. It is a pathology comparison and does not test any treatment, cure or prevention.
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.
- Performance of plasma p-tau217 for the detection of amyloid-β positivity in a memory clinic cohort using an electrochemiluminescence immunoassay
- Incidence of Alzheimer's disease in a rural community in India: the Indo-US study
- Incorporating ethnicity into genetic risk assessment for Alzheimer disease: the REVEAL study experience
- In vivo staging of regional amyloid deposition
- Effect of vitamin E and memantine on functional decline in Alzheimer disease: the TEAM-AD VA cooperative randomized trial
- Classifications of Neurodegenerative Disorders Using a Multiplex Blood Biomarkers-Based Machine Learning Model
- Markers of microglia in post-mortem brain samples from patients with Alzheimer's disease: a systematic review
- Hormone replacement therapy and incidence of Alzheimer disease in older women: the Cache County Study
- The Evolution of Randomized Clinical Trial Designs to Assess Therapeutics in Alzheimer Disease
- Idebenone, a new drug in the treatment of cognitive impairment in patients with dementia of the Alzheimer type