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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Neuroimaging with iron-sensitive MR sequences [gradient echo T2* and susceptibility-weighted imaging (SWI)] identifies small signal voids that are suspected brain microbleeds.
Why it matters
This postmortem MRI study correlated signal voids seen on iron-sensitive imaging with tissue pathology in brains with Alzheimer's disease and varying degrees of cerebral amyloid angiopathy. It addresses how to interpret these imaging findings, not how to treat, cure, or prevent Alzheimer's disease.
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Mild cognitive impairment (MCI) is a nosological entity proposed as an intermediate state between normal aging and dementia.
Why it matters
In a small study of 45 people, blood markers of oxidative stress were altered similarly in those with mild cognitive impairment and Alzheimer's disease compared to healthy controls. This suggests oxidative stress occurs early, but the study does not show that treating it changes the disease course.
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48/100
A sensitive marker for monitoring progression of early Alzheimer's disease would help to develop and test new therapeutic strategies.
Why it matters
This study found that people with amnestic mild cognitive impairment who converted to Alzheimer's disease had greater metabolic decreases in certain brain regions than those who did not convert. The findings describe brain changes associated with progression to Alzheimer's disease but do not test any treatment or prevention.
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Oxidative stress has been implicated in the pathogenesis of a number of diseases including Alzheimer's disease (AD).
Why it matters
This review summarizes findings that proteins in the brain are oxidatively modified in Alzheimer's disease, mild cognitive impairment, and animal models, supporting a role for amyloid beta in this process. It is a review of laboratory and tissue findings and does not show that any treatment targeting oxidative stress works in patients.
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48/100
Infectious agents have been proposed as potential causes of Alzheimer's disease (AD).
Why it matters
This study examined whether eradicating Helicobacter pylori infection affected cognitive and functional status in patients with Alzheimer's disease, after finding a high prevalence of the infection in these patients. It tests an infection treatment for possible benefit in Alzheimer's disease, but the available text does not report the outcome.
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The introduction of immunotherapy and its ultimate success will require re-evaluation of the pathogenesis of Alzheimer's disease particularly with regard to the role of the ageing microvasculature and the effects of APOE genotype.
Why it matters
This review discusses how ageing brain arteries and cerebral amyloid angiopathy affect the removal of amyloid beta along perivascular pathways, and notes that immunotherapy success will require re-evaluating this. It is a discussion of disease mechanisms and their potential impact on therapy, not a tested treatment, cure or prevention.
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Alzheimer's disease is a major cause of dementia in humans.
Why it matters
In a mouse model of Alzheimer's disease, weekly injections of M-CSF prevented cognitive loss and reduced amyloid deposits, and stabilized cognitive decline in mice that already had amyloid pathology. These are animal findings only and have not been shown to treat or prevent Alzheimer's disease in people.
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Cerebrospinal fluid (CSF) concentrations of amyloid-beta (Abeta) 1-38, 1-40, 1-42, total-tau and phospho-tau in samples from 156 patients with Alzheimer's disease (AD) (n = 44), depressive cognitive complainers (DCC, n = 25) and various other forms of non-Alzheimer dementias (NAD, n = 87) were analyzed by electrochemiluminescence and enzyme linked immunosorbent assay, respectively.
Why it matters
This study analyzed several cerebrospinal fluid amyloid-beta and tau markers, alone and in combination, to see how well they diagnose Alzheimer disease and distinguish it from other dementias. It is a diagnostic study and does not test any treatment, cure, or prevention.
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48/100
Simple MRI biomarkers, in addition to their diagnostic use, have a prognostic value with respect to mortality in a memory clinic population.
Why it matters
In 1,138 memory clinic patients, certain MRI markers such as white matter hyperintensities and microbleeds predicted mortality after adjusting for age, sex, and diagnosis. This is an observational study about predicting death and does not test any treatment for Alzheimer's disease.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder that destroys patient memory and cognition, communication ability with the social environment and the ability to carry out daily activities.
Why it matters
This review suggests that lipoic acid may serve as an anti-inflammatory and neuroprotective treatment for Alzheimer's disease, noting that a neuroprotective treatment for early stages remains unavailable for clinical use. It is a suggestion based on a review, not evidence that lipoic acid treats, cures or prevents the disease.
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Low and high thyrotropin levels were associated with an increased risk of incident AD in women but not in men.
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Alzheimer's disease is the commonest dementia.
Why it matters
This review describes how amyloid-beta deposits in the basement membranes of cerebral capillaries and arteries correspond to perivascular drainage pathways that eliminate interstitial fluid from the brain, and how failure of this drainage relates to cerebral amyloid angiopathy and Alzheimer's disease. It presents a proposed mechanism and reports no treatment, cure or prevention.
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This study confirms previous reports of potentially hazardous driving in persons with early Alzheimer disease, but also indicates that some individuals with very mild dementia can continue to drive safely for extended periods of time.
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Accumulating evidence suggests insulin and insulin signaling may be involved in the pathophysiology of Alzheimer disease (AD).
Why it matters
In people with early Alzheimer's disease, higher peripheral insulin levels were associated with less brain atrophy, less cognitive dysfunction, and lower dementia severity. This suggests insulin signaling may play a role in the disease, but the study does not show that giving insulin helps.
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Understanding the mechanisms of amyloid-beta protein (Abeta) production and clearance in the brain has been essential to elucidating the etiology of Alzheimer disease (AD).
Why it matters
This study tested whether ex vivo gene delivery of an amyloid-beta-degrading protease could enhance clearance of amyloid beta in the brain and reduce plaque burden. It notes that no disease-modifying agents of this kind have achieved clinical validation, so it does not show a treatment that works in patients.
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The National Alzheimer's Coordinating Center (NACC) is responsible for developing and maintaining a database of participant information collected from the 29 Alzheimer's Disease Centers (ADCs) funded by the National Institute on Aging (NIA).
Why it matters
Describes the Uniform Data Set, a standard set of assessments collected over time from participants at the 29 Alzheimer's Disease Centers funded by the National Institute on Aging. It is meant to help compare people with mild Alzheimer's and mild cognitive impairment with people without dementia.
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48/100
Population-based brain mapping provides great insight into the trajectory of aging and dementia, as well as brain changes that normally occur over the human life span.
Why it matters
This paper describes three brain mapping techniques that can measure the spread of brain shrinkage over time and track disease progression in drug trials. It is about tools for monitoring, not about a treatment, cure, or prevention.
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Microglial activation is a key feature in Alzheimer's disease and is considered to contribute to progressive neuronal injury by release of neurotoxic products.
Why it matters
In this laboratory work, a loss-of-function mutation in the Tlr4 gene reduced microglial and monocytic activation by aggregated amyloid peptide and lowered release of inflammatory products. These are cellular and animal findings and do not establish any treatment or prevention for people.
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Brain zinc accumulation is a prominent feature of advanced Alzheimer disease (AD) and is biochemically linked to brain amyloid beta-peptide accumulation and dementia severity in AD.
Why it matters
In postmortem brain tissue from 10 Alzheimer patients and other groups, zinc was more than doubled in the Alzheimer-affected cortex and rose with amyloid levels and dementia severity. This is a small autopsy study and does not show whether zinc causes Alzheimer's disease or could be a treatment target.
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48/100
The degree of coronary artery disease is independently associated with the cardinal neuropathological lesions of Alzheimer disease.
Why it matters
In autopsied brains, more coronary artery disease was linked to more Alzheimer-type plaques and tangles, and this link was stronger in APOE4 carriers. This is an autopsy association and cannot show that heart disease causes Alzheimer pathology or that treating it prevents it.
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Anosognosia in those with Alzheimer's disease is manifested as poor awareness of deficits in iADL and bADL, depressive changes and behavioural disinhibition.
Why it matters
This study describes a way to diagnose anosognosia (poor awareness of one's own deficits) in Alzheimer's disease by comparing caregiver and patient reports, especially about instrumental daily activities. It found that this lack of awareness becomes more common as dementia gets more severe, which matters for how care is assessed and managed.
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48/100
Magnetic resonance imaging-based volumetric measurements provide a useful technique for quantifying in vivo regional cerebral atrophy in Alzheimer disease (AD).
Why it matters
In this small study of 10 familial Alzheimer disease patients and 10 matched controls, all four cingulate regions were significantly smaller in Alzheimer disease cases, with the posterior cingulate showing the greatest atrophy. The authors suggest that detecting and monitoring this atrophy may provide insights into the natural history of Alzheimer disease.
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The proteases (secretases) that cleave amyloid-beta (Abeta) peptide from the amyloid precursor protein (APP) have been the focus of considerable investigation in the development of treatments for Alzheimer disease.
Why it matters
In a transgenic mouse model, suppressing beta-amyloid production after amyloid had already formed did not clear the existing amyloid deposits, which persisted. This animal study suggests that simply stopping new amyloid production may not remove established lesions, but it does not test this in people.
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The differential response to cholinergic challenge in mild cognitive impairment and Alzheimer patients may reflect a difference in the functional status of the cholinergic system between both groups, which is in line with recent results showing a differential clinical response to cholinergic treatment.
Why it matters
This pharmacological fMRI study found that a cholinergic challenge affected hippocampal activation differently in people with mild cognitive impairment and people with Alzheimer's disease. It suggests a difference in the cholinergic system between these groups, but it does not test a treatment, cure, or prevention.
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As our population ages, the incidence and prevalence of Alzheimer disease (AD) will increase dramatically.
Why it matters
This review found good evidence that cholinesterase inhibitors and memantine are modestly effective for treating Alzheimer's disease, with memantine effective in late stage disease. It found insufficient evidence to recommend ginkgo biloba, estrogen, statins or nonsteroidal anti-inflammatory drugs for prevention or treatment, and vitamin E was supported by only a single trial.
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.
- Age and diagnostic performance of Alzheimer disease CSF biomarkers
- National Institute on Aging-Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease
- Aggregation of vascular risk factors and risk of incident Alzheimer disease
- Associations of Plasma Phospho-Tau217 Levels With Tau Positron Emission Tomography in Early Alzheimer Disease
- Targeted proteomic biomarker profiling using NULISA in a cohort enriched with risk for Alzheimer's disease and related dementias
- Comprehension of metaphors and idioms in patients with Alzheimer's disease: a longitudinal study
- Serum cholesterol and risk of Alzheimer disease: a community-based cohort study
- Low cerebrospinal fluid concentration of mitochondrial DNA in preclinical Alzheimer disease
- Alzheimer Detection Using Deep Learning Methods
- Alzheimer disease brain atrophy subtypes are associated with cognition and rate of decline