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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40/100
In adults with DS, early amyloid-β accumulation in the striatum is divergent from sporadic AD; however, despite the early striatal amyloid-β, glucose hypometabolism was confined to the typical AD-associated regions, which occurs similarly in autosomal dominant AD.
Why it matters
In 24 adults with Down syndrome, this imaging study found that amyloid buildup in the striatum happened earlier than in typical Alzheimer's disease, but reduced glucose metabolism appeared in the brain regions usually affected in Alzheimer's. This suggests the sequence of brain changes in Down syndrome partly differs from sporadic Alzheimer's disease, though the study was small.
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There is growing evidence of the involvement of advanced glycation end products (AGEs) in the pathogenesis of neurodegenerative processes including Alzheimer's disease (AD) and their function as a seed for the aggregation of Aβ, a hallmark feature of AD.
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Alzheimer's disease (AD), the most common form of dementia, is a progressive disorder manifested by gradual memory loss and subsequent impairment in mental and behavioral functions.
Why it matters
This review discusses the gut-brain axis, the microbiome, leaky gut and bacterial translocation as possible mechanisms in Alzheimer's disease, alongside risk factors such as diabetes, hyperlipidemia, obesity, vascular factors and depression. It proposes mechanisms only and reports no treatment or prevention result.
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Acetylcholine (ACh) has a crucial role in the peripheral and central nervous systems.
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Down syndrome (DS) is a common genetic condition caused by the presence of three copies of chromosome 21 (trisomy 21).
Why it matters
This review describes mouse models used to study Alzheimer disease in Down syndrome and notes that not all people with Down syndrome who have Alzheimer neuropathology develop dementia. It discusses what future models need, but it does not report a treatment or prevention for Alzheimer disease.
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Our results suggest that DTI data provide better prediction accuracy than GM volume in predementia AD.
Why it matters
This study applied a support vector machine to diffusion tensor imaging and volumetric MRI data to distinguish mild cognitive impairment subjects by amyloid-β42 status and from healthy controls, with accuracies up to 77%. It is a prediction study and does not test any treatment, cure or prevention.
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Alzheimer's disease (AD) is the most common form of dementia and its prevalence is increasing.
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This review highlights the progression of biological changes underlying AD and their association with the clinical syndrome.
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Neurodegenerative diseases, such as Alzheimer disease, result in cognitive decline and dementia and are a leading cause of mortality in the growing elderly population.
Why it matters
This review describes how neuroimaging biomarkers, mainly regional atrophy on structural MRI, patterns of hypometabolism on 18F-FDG PET, and cerebral amyloid plaque detection on amyloid PET, can evaluate brain abnormalities to improve early diagnosis and help predict disease course in neurodegenerative dementias. It discusses the strengths and synergies of these techniques and some promising imaging methods under development, but it reports no treatment, cure, or prevention for Alzheimer's disease.
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Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by cognitive decline, brain atrophy due to neuronal and synapse loss, and formation of two pathological lesions: extracellular amyloid plaques, composed largely of amyloid-beta peptide (Aβ), and neurofibrillary tangles formed by intracellular aggregates of hyperphosphorylated tau protein.
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Alzheimer's disease (AD) is the most prevalent type of dementia.
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Amyloid beta (Aβ) is a peptide of 39-43 amino acids found in large amounts and forming deposits in the brain tissue of patients with Alzheimer's disease (AD).
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These measures offer a sensitive method of assessing spontaneous speech output in AD, and they discriminate well between people with AD and healthy older adults.
Why it matters
In older adults with and without Alzheimer's disease, measures such as percentage of voice breaks, number of voice periods and breaks, shimmer, and noise-to-harmonics ratio characterized people with Alzheimer's disease with 84.8% accuracy. The authors describe this as a promising tool for diagnosis and prognosis, not for treating, curing, or preventing Alzheimer's disease.
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40/100
We evaluated the brain metabolic correlates of main indexes of a widely used word list learning test, the Rey Auditory Verbal Memory Test (RAVLT), in a group of elderly subjects with memory complaints.
Why it matters
In older adults with memory complaints, brain glucose scans (FDG-PET) showed that delayed recall on a standard word-list test was tied to activity in the posterior cingulate and precuneus, and long-term retention also to orbitofrontal areas. Immediate recall scores showed no such link. The authors say these regions overlap those affected in the earliest stages of Alzheimer-type brain changes, helping map where memory problems begin.
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Loss of memory is among the first symptoms reported by patients suffering from Alzheimer's disease (AD) and by their caretakers.
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Alzheimer's disease is the commonest cause of dementia in the elderly, but its pathological determinants are still debated.
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Blood-brain barrier (BBB) regulates transport of various molecules and maintains brain homeostasis.
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In Alzheimer's disease (AD), structural and functional brain network organization is disturbed.
Why it matters
This small study used magnetoencephalography and graph spectral analysis to detect disrupted functional brain networks in people who already had Alzheimer's disease. It is a technical method for measuring network changes, not a treatment, cure, or prevention for Alzheimer's disease.
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The pathological hallmarks of Alzheimer's disease (AD)--widespread synaptic and neuronal loss and the pathological accumulation of amyloid-beta peptide (Aβ) in senile plaques, as well as hyperphosphorylated tau in neurofibrillary tangles--have been known for many decades, but the links between AD pathology and dementia and effective therapeutic strategies remain elusive.
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Granulovacuolar degeneration (GVD) is characterized by the presence of vacuolar cytoplasmic lesions in nerve cells of the medial temporal lobe.
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Research suggests that Alzheimer disease (AD) pathophysiology begins prior to the clinical expression of the disease and that biomarker measures may provide direct evidence of this process.
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Growing evidence suggests that type 2 diabetes mellitus (DM) is associated with age-dependent Alzheimer's disease (AD), the latter of which has even been considered as type 3 diabetes.
Why it matters
In cell and rat models of diabetes-related Alzheimer-like changes, exendin-4, a GLP-1 receptor agonist, showed protective effects. This is early laboratory and animal work and does not establish any treatment, cure or prevention for people.
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The combination of decreased cerebrospinal fluid (CSF) levels of beta-amyloid (1-42) and increased levels of phosphorylated tau (ptau-181) or total tau protein are known to be biomarkers ofAlzheimer's disease (AD).
Why it matters
This study evaluated whether cerebrospinal fluid amyloid, phosphorylated tau and total tau could distinguish Alzheimer's disease from non-Alzheimer dementia in 30 Thai patients. It is about using biomarkers for diagnosis, not about treating, curing or preventing the disease.
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Alzheimer's disease (AD) is a neurodegenerative disease with major clinical hallmarks of memory loss, dementia, and cognitive impairment.
Why it matters
This review discusses astrocytes and their possible involvement in the neuroinflammatory pathogenesis of Alzheimer's disease, noting that cytokines can play both neuroprotective and other roles. It offers no treatment, cure or prevention.
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Cognitive impairment is prevalent in older schizophrenia patients but its biological basis is unknown.
Why it matters
In a small group of older schizophrenia patients, cerebrospinal fluid markers of amyloid and neurodegeneration were measured and related to cognition and MRI findings. The study was exploratory and does not establish whether these markers reflect Alzheimer disease pathology or guide treatment in this group.
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.
- [alpha]-Secretase ADAM10 as well as [alpha]APPs is reduced in platelets and CSF of Alzheimer disease patients
- Diversity of Amyloid-beta Proteoforms in the Alzheimer's Disease Brain
- Neurodevelopmental Vulnerability in Alzheimer's Disease and Frontotemporal Dementia
- Prevalence and prognosis of Alzheimer's disease at the mild cognitive impairment stage
- Independent information from cerebrospinal fluid amyloid-β and florbetapir imaging in Alzheimer's disease
- Ambient air pollution and Alzheimer’s disease and other dementias: a global study between 1990 and 2019
- Retinal biomarkers for the risk of Alzheimer’s disease and frontotemporal dementia
- Sex Differences in Associations of Lewy Body Disease with Alzheimer's Disease and Cognitive Decline
- Novel Alzheimer risk genes determine the microglia response to amyloid-β but not to TAU pathology
- Polygenic risk score analysis of pathologically confirmed Alzheimer disease