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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Prior MR imaging studies, primarily at 1.5T, established hippocampal atrophy as a biomarker for Alzheimer disease. 3T MR imaging offers a higher contrast and signal-to-noise ratio, yet distortions and intensity uniformity are harder to control.
Why it matters
This study compared 1.5T and 3T MRI for mapping hippocampal atrophy in people with Alzheimer's disease, mild cognitive impairment and healthy controls. It is about improving an imaging biomarker for diagnosis, not about treating, curing or preventing Alzheimer's disease.
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FDG-PET and amyloid PET imaging are valuable in the assessment of patients with Alzheimer's disease.
Why it matters
The review states that FDG-PET and amyloid PET imaging are valuable in assessing patients with Alzheimer's disease, and that amyloid PET may exclude significant amyloid deposition and thus Alzheimer's disease in an appropriate clinical setting. It concerns diagnosis only, not treating, curing or preventing the disease.
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All measures distinguished the dementia and control groups and all markers associated with the cognitive test scores.
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However, interventions that minimize caregiver distress and improve patient functioning may impact on both subjective and objective burden.
Why it matters
In 1,497 people with Alzheimer's living at home in France, Germany and the UK, caregivers of people with more advanced disease reported higher burden on the Zarit Burden Interview and spent more time on care, including supervision. The authors found that how burdened a caregiver feels and how many hours they spend caregiving "are influenced by different factors", so both need attention when trying to reduce the load. These are associations at a single time point, not a tested intervention, and they say nothing about treating Alzheimer's itself.
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Alzheimer disease (AD) is the most common form of dementia among the elderly and is characterized by progressive loss of memory and cognition.
Why it matters
This review proposes that oxidative stress links type 2 diabetes to Alzheimer's disease and describes molecular mechanisms such as amyloid-beta driving reactive oxygen and nitrogen species. It is a mechanistic review, not a clinical trial, so it does not show that any treatment prevents or cures Alzheimer's disease.
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The objective of this analysis was to develop a nonlinear disease progression model, using an expanded set of covariates that captures the longitudinal Clinical Dementia Rating Scale-Sum of Boxes (CDR-SB) scores.
Why it matters
This analysis developed a nonlinear disease progression model for Clinical Dementia Rating-Sum of Boxes scores using 301 Alzheimer's and mild cognitive impairment patients from ADNI-1 followed for 2-3 years. It is a modeling study of disease progression and does not test any treatment, cure, or prevention.
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47/100
Accumulation of amyloid-β in cerebral blood vessels occurs in familial and sporadic forms of cerebral amyloid angiopathy and is a prominent feature of Alzheimer disease.
Why it matters
Using transgenic mice with amyloid precursor protein mutations, the study examined how cerebral amyloid angiopathy affects cerebrovascular structure and function with age. It is animal-model research and does not establish any treatment, cure, or prevention for Alzheimer's disease.
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47/100
Post-operative cognitive dysfunction (POCD) is associated with increased cost of care, morbidity, and mortality.
Why it matters
In mice, this study investigated whether peripheral surgery causes age-dependent postoperative cognitive impairment and Alzheimer-related neuropathology. It is animal work on the causes of postoperative cognitive dysfunction and does not test a treatment, cure, or prevention for Alzheimer's disease.
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High serum/plasma cholesterol levels have been suggested as a risk factor for Alzheimer's disease (AD).
Why it matters
This review argues that the hypothesis that cholesterol causes Alzheimer's disease is debatable, noting that the strongest causal evidence comes from experimental studies while there are problems with the hypothesis, including cholesterol levels in serum and brain of patients. It does not conclude that lowering cholesterol prevents or treats Alzheimer's disease.
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Alzheimer's disease (AD) represents the main form of dementia, and is a major public health problem.
Why it matters
This review states that current Alzheimer's treatments give only marginal symptom relief and there are no effective disease-modifying or preventive interventions. It describes how genetic research is being used to find biomarkers and drug targets, not a treatment.
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For prediction of dementia in MCI, the AD signature cortical thickness biomarker performed better than hippocampal volume.
Why it matters
For predicting dementia in mild cognitive impairment, an MRI measure of Alzheimer's signature cortical thickness performed better than hippocampal volume, and both this MRI marker and cerebrospinal fluid amyloid-beta were useful in predicting time to diagnosis. This is a biomarker comparison study and does not show that any treatment, cure, or prevention works.
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Our results revealed disease severity-related alterations of the thalamo-default mode network and thalamocortical connectivity in AD and MCI patients.
Why it matters
Patients with Alzheimer's disease showed decreased functional connectivity between the thalamus and several brain regions compared with normal controls, and the strength of connectivity correlated with clinical variables. These findings reveal disease severity-related alterations of the thalamo-default mode network and thalamocortical connectivity.
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Alzheimer's disease (AD) is the most common cause of dementia worldwide.
Why it matters
This review notes that only acetylcholinesterase inhibitors and memantine are currently approved, and these give symptom relief rather than modifying the disease. It describes amyloid- and tau-based approaches as still under development, with many candidate drugs having failed in clinical testing.
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Amyloid PET imaging is a novel diagnostic test that can detect in living humans one of the two defining pathologic lesions of Alzheimer disease, amyloid-β deposition in the brain.
Why it matters
This task force update clarifies appropriate use criteria for amyloid PET imaging, including which patients with mild cognitive impairment may be suitable and how to educate clinicians. It concerns diagnosis and does not test any treatment, cure or prevention.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder that accounts for the major cause of dementia, and the increasing worldwide prevalence of AD is a major public health concern.
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With tract-based spatial statistics and region-of-interest analyses, increased diffusivity in the extra-axonal space (extra-axonal axial and radial diffusivities) in several white matter tracts sensitively and accurately discriminated healthy controls from those with amnestic mild cognitive impairment (area under the receiver operating characteristic curve = 0.82-0.95), while widespread decreased axonal water fraction discriminated amnestic mild cognitive impairment from Alzheimer disease (area under the receiver operating characteristic curve = 0.84).
Why it matters
Novel white matter tract integrity metrics from diffusion kurtosis imaging discriminated healthy controls from amnestic mild cognitive impairment and amnestic mild cognitive impairment from Alzheimer's disease with good accuracy. These metrics were also correlated with processing speed, suggesting they may be sensitive to disease progression, but this was a small study.
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We examined differences in cerebral blood flow (CBF) measured by Arterial Spin Labeled perfusion MRI (ASL MRI) across the continuum from cognitively normal (CN) older adults to mild Alzheimer's Disease (AD) using data from the multi-site Alzheimer's Disease Neuroimaging Initiative (ADNI).
Why it matters
Using arterial spin labeled MRI, this multi-site study found lower cerebral blood flow in late mild cognitive impairment and Alzheimer's disease compared with cognitively normal older adults. It is an imaging study of blood flow and does not test any treatment, cure, or prevention.
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Human apolipoprotein E (apoE) has 3 isoforms: apoE2, apoE3, and apoE4.
Why it matters
This review proposes that apoE4 has direct harmful effects on blood vessels in the brain, which could then lead to nerve cell damage and reduced clearance of amyloid. It is a hypothesis based on reviewed data and does not report any treatment or prevention.
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Amyloid imaging studies of presymptomatic familial Alzheimer's disease have revealed the striatum and thalamus to be the earliest sites of amyloid deposition.
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Alzheimer's disease (AD) is the most common cause of dementia among older people.
Why it matters
In a mouse model of Alzheimer's disease, inactivating monoacylglycerol lipase suppressed beta-amyloid production and accumulation and prevented neuroinflammation. This is an animal study, so it does not yet show that targeting this enzyme treats or prevents Alzheimer's disease in people.
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Alzheimer's disease (AD) is the most prevalent form of dementia with an estimated worldwide prevalence of over 30 million people, and its incidence is expected to increase dramatically with an increasing elderly population.
Why it matters
This study used a metabolomics method on cerebrospinal fluid to try to predict whether people with mild cognitive impairment would progress to Alzheimer's disease. It correctly classified most samples in the main analysis and reached 83% accuracy in a small blind test set, but the authors describe this as a potentially useful tool rather than a proven test.
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Alzheimer's disease is the leading cause of dementia in the elderly and is defined by two pathological hallmarks; the accumulation of aggregated amyloid beta and excessively phosphorylated Tau proteins.
Why it matters
This review discusses how copper, zinc and iron can promote amyloid-beta oligomer formation and generate reactive oxygen species, and suggests that disturbed metal homeostasis may underlie an increased oxidative stress burden in Alzheimer's disease. It describes possible molecular links and mechanisms, not a proven treatment, cure or prevention.
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Research progress has provided detailed understanding of the molecular pathogenesis of Alzheimer disease (AD).
Why it matters
This review chapter discusses cerebrospinal fluid and plasma biomarkers for Alzheimer disease and the need to detect the disease in its predementia phase, because drugs will probably work only if neurodegeneration is not too advanced. It is a review of biomarkers and does not report a tested treatment, cure, or prevention.
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These results suggest that increased baseline hallucinations, apathy and anxiety are associated with current and future disease progression in AD.
Why it matters
In 812 older adults followed for three years, hallucinations, anxiety and apathy were associated with greater functional impairment at the start and over time, while delusions, agitation, depression and several other symptoms were not significantly associated with global functioning. These findings describe which symptoms track with disease progression but do not show that treating them changes the course of Alzheimer's disease.
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47/100
The proteolytic processing of amyloid precursor protein (APP) to generate the neurotoxic amyloid β (Aβ) peptide is central to the pathogenesis of Alzheimer disease (AD).
Why it matters
This study identified variants in genes regulating retromer function, a protein complex needed to retrieve SorL1, which is genetically linked to Alzheimer's disease. It is genetic work on disease risk and reports no 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.
- Behavioral and neuronal substrates of serious game‐based computerized cognitive training in cognitive decline related to Alzheimer's Disease
- Melatonin fails to improve sleep or agitation in double-blind randomized placebo-controlled trial of institutionalized patients with Alzheimer disease
- Assessment of Plasma Total Tau Level as a Predictive Biomarker for Dementia and Related Endophenotypes
- Coping strategies, anxiety and depression in caregivers of people with Alzheimer's disease
- Correlation of In Vivo [18F]Flortaucipir With Postmortem Alzheimer Disease Tau Pathology
- Education and Alzheimer Disease Genetic Risk in Associations of GLP-1 Receptor Agonists With Dementia Among Adults With Type 2 Diabetes
- Brain Imaging and Blood Biomarker Abnormalities in Children With Autosomal Dominant Alzheimer Disease: A Cross-Sectional Study
- Research Proposal Consciousness Mode Alzheimers
- Poor self-rated health did not increase risk of permanent nursing placement or mortality in people with mild Alzheimer's disease
- S100 beta protein expression in Alzheimer disease: potential role in the pathogenesis of neuritic plaques