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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For 11 AD cases and four normal elderly controls, post mortem volumes of the hippocampal subdivisions were calculated by using magnetic resonance imaging and histological sections.
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Epidemiological and clinical studies suggest that nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit cyclooxygenase (COX) slow the progression and delay the onset of Alzheimer disease (AD).
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Alzheimer's disease (AD) and Lewy body disease (LBD) are the most common causes of dementia in the elderly population.
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Anxiety symptoms were common and significantly related to ADL and additional neuropsychiatric problems in this sample.
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Delayed memory impairments and medial temporal-lobe atrophy are considered to be cardinal features of Alzheimer's disease (AD).
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The present study examined the relationship between visual attention measures and driving performance in healthy older adults and individuals with very mild and mild dementia of the Alzheimer type (DAT).
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The hypothesis is forwarded that sporadic late-onset Alzheimer disease is caused by non-insulin dependent diabetes mellitus which is confined to the brain.
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Patients with Alzheimer disease (AD) show visual impairments in color discrimination (blue hues), stereoacuity, and contrast sensitivity.
Why it matters
In 22 adults with Down syndrome compared with 18 adults with mental retardation of non-Down syndrome cause, the Down syndrome group showed more tritanomalous color errors, higher stereoacuity thresholds and reduced contrast sensitivity, resembling visual deficits seen in Alzheimer disease. The authors suggest these deficits may appear before and independently of age-associated dementia, but this is a small study and not a treatment or prevention finding.
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High-fidelity driving simulation provides a unique new source of performance parameters to standardize the assessment of driver fitness.
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While apolipoprotein E (ApoE) and beta-amyloid (A beta) co-localize in senile plaques in cortex and cerebellum in Alzheimer disease (AD), the A beta-positive, predominantly diffuse plaques in the striatum do not exhibit ApoE immunoreactivity regardless of disease duration.
Why it matters
In autopsy brain tissue, reactive astrocytes around infarcts produced apolipoprotein E, but astrocytes around neuritic plaques in Alzheimer's disease did not label with apolipoprotein E, and plaque apolipoprotein E followed beta-amyloid instead. This is a tissue study describing where apolipoprotein E appears in the brain and does not test any treatment, cure or prevention.
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Activated microglia, overexpressing interleukin-1 (IL-1), and activated astrocytes, overexpressing S100beta, have been implicated in the formation and evolution of tau2-immunoreactive (tau2+) neuritic plaques in Alzheimer disease.
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36/100
In vivo imaging of patients with Alzheimer's disease using positron emission tomography (PET) demonstrates progressive reductions in brain glucose metabolism and blood flow in relation to dementia severity, more so in association than primary cortical regions.
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The neurodegeneration and amyloid deposition of sporadic Alzheimer disease (AD) also occur in familial AD and in all trisomy-21 Down syndrome (DS) patients, suggesting a common pathogenetic mechanism.
Why it matters
This cell study found abnormal chromatid break tests after fluorescent light irradiation in cells from all tested Down syndrome, sporadic Alzheimer and familial Alzheimer patients, unlike most normal donors. The authors suggest the test might help predict inherited familial Alzheimer disease, but it is a laboratory assay and not a treatment, cure or prevention.
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Alzheimer's disease (AD) is characterized by a progressive cognitive decline in which memory, initiation, learning and conceptualization are severely affected.
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Alzheimer disease (AD) is characterized by deposits of an aggregated 42-amino-acid beta-amyloid peptide (beta AP) in the brain and cerebrovasculature.
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The olfactory bulb (OB), with its comparatively simple and well-delineated connectivity, presents an interesting system for examining cell-specific pathology in neurologic degenerative disorders such as Alzheimer's disease (AD).
Why it matters
In Alzheimer disease, the large efferently projecting mitral cells of the olfactory bulb were found to degenerate, and in some cases olfactory nerve terminals showed hyperplasia with focal accumulations of beta-amyloid immunoreactivity. This is a pathological description of the olfactory bulb in Alzheimer disease, not a treatment, cure or prevention.
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The dementia of Alzheimer disease (AD) correlates with the deposition of extracellular amyloid, and this amyloid arises from the abnormal processing of a high molecular weight amyloid peptide precursor (APP), which is a normal cellular protein that is found in both brain and in peripheral tissues in humans.
Why it matters
This study developed a two-site immunoradiometric assay that could measure amyloid peptide precursor in human blood, finding it present in plasma at a mean concentration of 32 pM. There was no significant difference in APP concentration among 25 controls, 19 Alzheimer's disease patients, and 10 individuals with Down syndrome, so the assay did not distinguish these groups.
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Expression of major histocompatibility complex (MHC) class I (HLA-A,B,C) and class II (HLA-DR) antigens was studied in postmortem brain tissue of Alzheimer's disease and age-matched control cases.
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Patients with Down syndrome (DS) over 40 years of age, prematurely and consistently develop neurofibrillary tangles (NFT), intracytoplasmic inclusions of highly insoluble straight or paired helical 12-16 nm filaments, and senile plaques (SP) composed of abnormal neurites surrounding a core of beta amyloid.
Why it matters
This review notes that people with Down syndrome consistently develop the same amyloid plaques and tau tangles seen in Alzheimer's disease, often before age 40. However, it reports that studies trying to link these brain lesions to actual dementia have produced conflicting results, so the presence of plaques and tangles did not always match whether a person had dementia.
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The actual presence of the predicted precursor of Alzheimer's disease amyloid A4 protein, reported by Kang et al. (1987) in the Alzheimer brain, has yet to be verified.
Why it matters
This laboratory study found that the amyloid in senile plaques contains a larger polypeptide than the A4 protein, and that the C-terminal part of the precursor may exist in degenerated neurites in the plaques. It is early, tissue-based work and does not test any treatment, cure, or prevention.
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Alzheimer's disease is a neurodegenerative disorder characterized by global cognitive decline.
Why it matters
This genetic study mapped the amyloid beta precursor gene to chromosome 21 and showed through linkage analysis that the amyloid gene and the familial Alzheimer's disease gene are separate genetic loci. It clarifies the genetics of Alzheimer's disease but does not provide a treatment or cure.
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Although the precise role of astrocytes in the pathogenesis of Alzheimer's disease (AD) is currently undefined, studies carried out at the molecular level may lead to new insights into the functioning of this class of brain cells in dementia.
Why it matters
This study describes a lab method showing that messenger RNA for the astrocyte marker GFAP stays intact in brain tissue after death in Alzheimer's disease. It is a methods paper about tissue handling and provides no information about treating, curing, or preventing the disease.
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Patterns of discourse--as reflected in the use of propositions, cohesion devices, and in judgments of coherence--in the speech of 6 well elderly and 6 patients with senile dementia of the Alzheimer type (SDAT) during topic-centered interviews were compared.
Why it matters
This small study compared speech patterns in 6 people with senile dementia of the Alzheimer type and 6 well elderly people, finding differences in coherence and cohesion disruptions. It describes language features of the disease and does not test any treatment, cure or prevention.
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Multiple sclerosis (MS) is a neurodegenerative disease characterized by inflammatory demyelination and axonal injury.
Why it matters
In 100 multiple sclerosis patients, structural MRI features such as lesion distribution and central vein sign did not differ by Alzheimer's disease biomarker status, while longer exposure to B cell-depleting anti-CD20 therapies was associated with AD biomarkers. Only a small subset of 7 patients had biomarker evidence of Alzheimer's disease, so these findings are preliminary.
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Accurate prediction of the progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD) is essential for early intervention and effective disease management.
Why it matters
A hybrid deep learning and machine learning framework combining structural MRI and neurocognitive assessments predicted conversion from mild cognitive impairment to Alzheimer's disease up to three years in advance with 88.11% accuracy. This is a prediction tool, not a treatment, cure or prevention.
From across this topic
9 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 9. The same 9 appear here every time.
- Inhomogeneous distribution of Alzheimer pathology along the isocortical relief. Are cortical convolutions an Achilles heel of evolution?
- Effectiveness of a condensed protocol for disclosing APOE genotype and providing risk education for Alzheimer disease
- Functional correlates of TSH, fT3 and fT4 in Alzheimer disease: a F-18 FDG PET/CT study
- Causative and susceptibility genes for Alzheimer's disease: a review
- Neuropsychological and clinical indicators of Lewy body and Alzheimer's pathology
- Alzheimer's Disease in Down Syndrome
- Escitalopram for agitation in Alzheimer's dementia: a randomized controlled phase 3 trial
- Comparison of 7.0-T T₂*-magnetic resonance imaging of cerebral bleeds in post-mortem brain sections of Alzheimer patients with their neuropathological correlates
- Leveraging Artificial Intelligence in the Diagnosis of Neurodegenerative Disorders (Alzheimer's and Dementia) and in Managing Medication Schedules"