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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Sample statistics were computed from ADNI cohorts with no cognitive diagnosis, a diagnosis of mild cognitive impairment (MCI), and a diagnosis of possible or probable Alzheimer's disease (AD).
Why it matters
This study explored different definitions of intra-individual variability on the Mini Mental State Exam and Clock Drawing Test and compared their ability to distinguish cognitive groups and predict change in ADNI participants. It is about cognitive measurement methods, not treating, curing, or preventing Alzheimer's disease.
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The role of hypoperfusion in Alzheimer's disease (AD) is a vital component to understanding the pathogenesis of this disease.
Why it matters
This review describes reduced blood flow in the brain in Alzheimer's disease, including in mild cognitive impairment and in healthy people at higher risk. It notes that it is still debated whether this reduced flow causes the disease or results from it, and it does not establish any treatment or prevention.
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Phosphorylation of tau protein is a critical event in the pathogenesis of Alzheimer's disease (AD).
Why it matters
This study examined whether phosphorylated and total tau species in saliva could serve as Alzheimer disease biomarkers, since obtaining cerebrospinal fluid is invasive. It is a biomarker study and does not test any treatment, cure, or prevention.
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NPS are common even in the early stages of AD.
Why it matters
In 240 patient-caregiver dyads, neuropsychiatric symptoms were present in 76.5% of patients with very mild Alzheimer's disease and 84.9% of those with mild to moderate disease, most often apathy, depression, irritability, and agitation. These symptoms were significantly associated with caregiver assessment of the patient's quality of life but not with patients' self-assessed quality of life, and caregiver depression also significantly influenced their ratings.
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Alzheimer's disease (AD) is accompanied by smell dysfunction, as measured by psychophysical tests.
Why it matters
This small imaging study compared brain activity in response to odors in 12 early-stage Alzheimer's patients and 13 nondemented controls. It is an early study of how the disease affects the sense of smell, not about treating, curing or preventing it.
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Changes in PCC functional connectivity comprised bidirectional alterations in the resting networks in AD-affected brains, and the impaired resting functional connectivity seemed to change with AD progression.
Why it matters
In 46 Alzheimer patients and 16 healthy volunteers, connectivity between the posterior cingulate cortex and several other regions was disrupted in all Alzheimer groups and worsened with disease stage. This is an observational imaging study and does not test any treatment or show that restoring connectivity would change the disease.
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Primary progressive aphasia (PPA) is a neurodegenerative disorder with language impairment as the primary feature.
Why it matters
In 14 patients with primary progressive aphasia and either pathologically confirmed Alzheimer's disease or consistent CSF biomarkers, all had a logopenic/phonological aphasia syndrome, and the authors propose it may be a unihemispheric presentation of Alzheimer's disease. This is a clinical and imaging characterization, not a treatment, cure, or prevention.
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Clinical trials of disease modifying drugs for Alzheimer's disease (AD) in patients with mild cognitive impairment (MCI) might benefit from enrichment with true AD cases.
Why it matters
This study tested whether using biomarkers could improve clinical trials of Alzheimer's drugs by selecting patients with mild cognitive impairment who truly have Alzheimer's disease. It is about trial design and does not show that any treatment works.
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We used a previously validated automated machine learning algorithm based on adaptive boosting to segment the hippocampi in baseline and 12-month follow-up 3D T1-weighted brain MRIs of 150 cognitively normal elderly (NC), 245 mild cognitive impairment (MCI) and 97 Dementia of the Alzheimer's type (DAT) ADNI subjects.
Why it matters
This study found no significant link between delayed recall and hippocampal shape in cognitively normal elderly, but did find associations in people with mild cognitive impairment and Alzheimer's dementia. It is about understanding how memory tests relate to brain structure and does not test any treatment, cure, or prevention.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is characterized pathologically by the presence of senile plaques, neurofibrillary tangles, and synapse loss.
Why it matters
This review summarizes evidence that oxidative stress, possibly triggered by amyloid beta-peptide, is involved in the progression of Alzheimer's disease from mild cognitive impairment to later stages. It suggests exploring these pathways may lead to therapies, but no treatment is tested or proven here.
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Alzheimer's disease (AD) is the most common neurodegenerative disorder that affects the elderly.
Why it matters
This review discusses how neuroinflammation and oxidative stress contribute to Alzheimer's disease pathogenesis. It highlights that amyloid-beta peptide oligomers accumulate extracellularly and are associated with reactive microglia and astrocytes as well as degeneration of neuronal processes.
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Increased public education about AD is needed in these communities.
Why it matters
Hispanic and Chinese female caregivers were more likely than white caregivers to believe Alzheimer's disease is a normal part of aging and can be diagnosed by a blood test. The authors say these beliefs may delay help-seeking and that more public education is needed in these communities.
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There are no empiric data to support guidelines for duration of therapy with antidementia drugs.
Why it matters
This study followed 641 probable Alzheimer's disease patients over 20 years and examined whether persistent use of cholinesterase inhibitors and/or memantine slows clinical progression. It suggests that persistent antidementia drug use may slow progression, but it is an observational study and does not show a cure or prevention.
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Elevated glucocorticoid concentrations, decreased hippocampal volume and frontal atrophy with poor cognitive function have been reported in the elderly but not extensively in Alzheimer's disease (AD).
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More than a dozen epidemiological studies have reported that reduced levels or intake of omega-3 fatty acids or fish consumption is associated with increased risk for age-related cognitive decline or dementia such as Alzheimer's disease (AD).
Why it matters
This review reports that higher intake or blood levels of DHA appeared protective for Alzheimer's disease in several observational studies, but three studies suggested the ApoE4 genotype limits that protection. It calls for clinical trials and does not show that omega-3 fatty acids prevent or treat dementia.
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Recent evidence has suggested a role for soluble oligomeric Abeta species in the pathology of Alzheimer's disease (AD).
Why it matters
Plaques are found even in people without dementia, so researchers asked whether smaller, soluble clumps of amyloid-beta track the disease better. In brain tissue from controls, people with senile degenerative changes and people with Alzheimer's, the study found that soluble "fibrillar oligomers" (detected by the OC antibody) were significantly raised in multiple brain regions of Alzheimer's patients. It is a tissue-measurement study that shows an association, not a cause, a diagnostic test or a treatment.
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The hippocampus is among the first structures affected in Alzheimer's disease (AD).
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Early Alzheimer's disease (EAD) is the intermediary stage between mild cognitive impairment (MCI) and late-stage Alzheimer's disease (AD).
Why it matters
In post-mortem brain tissue from people with early Alzheimer's disease, six proteins carried abnormally high amounts of HNE, a marker of lipid peroxidation (a type of oxidative damage), compared with age-matched control brain. These proteins work in antioxidant defense, communication between nerve cells, and energy metabolism, and they overlap with proteins previously found to be HNE-modified in mild cognitive impairment and late-stage Alzheimer's. The authors say this is "consistent with the hypothesis" that lipid peroxidation is an early event in Alzheimer's. It is an association in brain tissue from one brain region, not evidence about a cause, a test or a treatment.
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Studies suggest a link between bone loss and Alzheimer's disease.
Why it matters
People in the earliest stages of Alzheimer's disease had lower bone mineral density than non-demented controls, and lower bone density related to smaller brain volume and worse memory. This suggests a link between bone loss and early Alzheimer's, but it is an association and does not show that treating bone loss affects the disease.
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Retinas of transgenic mice harboring a mutant presenilin (PS1) and a mutant APP gene were processed for TUNEL and immunohistochemistry with antibodies against APP, amyloid-beta, monocyte chemotactic protein (MCP)-1, and F4/80.
Why it matters
In a mouse model of Alzheimer's disease, amyloid-beta deposits in the retina were linked to age-dependent increases in amyloid precursor protein and retinal degeneration. This is an animal study, so it does not yet show whether the same process happens in people or whether it can be treated.
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45/100
Caregivers with higher mastery had less NE reactivity to the stressor task.
Why it matters
In 69 elderly spousal Alzheimer caregivers, greater personal mastery was significantly associated with lower norepinephrine reactivity to an acute stressor. This concerns caregiver stress and cardiovascular risk, not the treatment, cure or prevention of Alzheimer's disease itself.
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Alzheimer disease is the most common cause of dementia and represents a major public health problem.
Why it matters
This review describes the genetics of Alzheimer's disease, including rare autosomal-dominant early-onset forms linked to mutations in amyloid precursor protein, presenilin 1 and presenilin 2, and the more common late-onset form assumed to be polygenic. It explains genetic factors but does not present a treatment, cure or prevention.
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There is a great interest in the relationship between Mild Cognitive Impairment (MCI) and the progression to Alzheimer's disease (AD).
Why it matters
In 34 people with mild cognitive impairment, 45 with Alzheimer's disease, and 28 controls, markers of oxidative stress were increased in both patient groups compared with controls, suggesting oxidative stress may be a signal of Alzheimer's pathology. It reports blood marker findings and does not show that any treatment, cure, or prevention works.
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As different signature changes associated with particular stages of disease burden are identified and validated, we anticipate expanded application of qEEG as a reliable and sensitive biomarker(s) of MCI and early Alzheimer's disease.
Why it matters
This review assesses quantitative electroencephalography and event-related potentials as possible biomarkers for mild cognitive impairment and early Alzheimer's disease. It describes these tools as relatively inexpensive, noninvasive and replicable, and anticipates expanded application as reliable biomarkers once signature changes are identified and validated.
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Increasing evidence supports a role for oxidative damage in the pathogenesis of Alzheimer's disease (AD).
Why it matters
This review reports that oxidative damage to fats, proteins, DNA, and RNA is increased in the brains of people with late-stage Alzheimer's disease and also in amnestic mild cognitive impairment, suggesting it happens early. It proposes oxidative damage as a possible target for slowing the disease, but no treatment is tested here.
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.
- Genetic predisposition to increased blood cholesterol and triglyceride lipid levels and risk of Alzheimer disease: a Mendelian randomization analysis
- The Role of Selected Bioactive Compounds in the Prevention of Alzheimer's Disease
- The Memory Alteration Test Is Correlated with Clinical, Cerebrospinal Fluid, and Brain Imaging Markers of Alzheimer Disease in Lima, Peru
- The genetic landscape of Alzheimer disease
- Enhanced Deep Learning Framework for Precise MRI ‐Based Alzheimer's Disease Stage Classification
- The clinical spectrum of cerebral amyloid angiopathy: presentations without lobar hemorrhage
- Aerobic glycolysis and tau deposition in preclinical Alzheimer's disease
- Hippocampal shape analysis of Alzheimer disease based on machine learning methods
- Association of graph network properties with Alzheimer's pathological hallmarks early in the disease continuum
- Machine learning–enhanced screening funnel for clinical trials in Alzheimer's disease