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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These findings contribute to the understanding of preclinical familial Alzheimer's disease and help set the stage for assessment of amyloid-modifying treatments in the prevention of familial Alzheimer's disease.
Why it matters
This cross-sectional imaging study looked at amyloid-beta deposition in people from a family with autosomal dominant Alzheimer's disease. The authors say the findings help set the stage for assessing amyloid-modifying treatments in preventing familial Alzheimer's disease, but no treatment was tested.
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Niney-two PD patients developed dementia, and 48 remained cognitively normal.
Why it matters
This 2012 study examined the brains of 140 people with Parkinson disease after death: 92 had developed dementia and 48 had stayed cognitively normal. Clumps of the protein α-synuclein (Lewy bodies and Lewy neurites) in the brain's outer layer, the cortex, were "the most significant correlate of dementia". The gene variant APOE4 "may independently influence the risk", and Alzheimer-type changes were "abundant in a subset of patients". This is an association found at autopsy, not proof of cause. The authors' suggestion that therapies aimed at these proteins "could potentially" help thinking was not tested in this study.
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Age is the strongest risk factor for sporadic Alzheimer disease (AD), yet the effects of age on rates of clinical decline and brain atrophy in AD have been largely unexplored.
Why it matters
Rates of clinical decline and brain atrophy in Alzheimer's disease and mild cognitive impairment decreased with older age, while healthy controls showed the opposite pattern. This implies that Alzheimer's appears milder in people older than about 85, which could make it harder to distinguish from normal aging and reduce the power of trials including older participants.
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Biomarker trajectory shapes by MMSE score were complex and were affected by interactions with age and APOE status.
Why it matters
This study characterized the trajectories of five major Alzheimer's biomarkers as they relate to cognitive scores, finding that biomarker values generally worsened with lower cognitive scores and that rates of change were associated with worsening cognition. It concludes that reliable models of full biomarker trajectories will require significant additional longitudinal data.
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In women, increased plasma adiponectin levels are an independent risk factor for the development of both all-cause dementia and AD.
Why it matters
In this long-term cohort study, after adjustment for other risk factors, only adiponectin in women was associated with an increased risk of all-cause dementia and Alzheimer's disease, with results at the borderline of statistical significance. It identifies a possible risk marker but does not show that any treatment or prevention targeting adiponectin changes the course of Alzheimer's disease.
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Even in a highly selected lifespan sample of adults, Aβ deposition is apparent in some adults and is influenced by APOE status.
Why it matters
In this study of cognitively normal adults, beta-amyloid deposition was found to vary across the cortex and increase with age, and higher amyloid burden was linked to poorer performance on some thinking tests. APOE epsilon 4 carriers had a higher rate of elevated amyloid.
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This article examines mechanisms of blood-brain barrier dysfunction in neurodegenerative disorders, notably Alzheimer's disease, and highlights therapeutic opportunities relating to these neurovascular deficits.
Why it matters
Covers neurovascular pathways to neurodegeneration in Alzheimer's disease and other disorders. It concerns how blood-vessel-related routes may contribute to nerve cell loss, and reports no treatment.
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A co-morbidity score was significantly higher in AD participants compared to controls.
Why it matters
This cross-sectional study found that people with a recent Alzheimer's disease diagnosis had a higher co-morbidity score and took more drugs than cognitively healthy controls, even after adjusting for co-morbidity. It is about drug burden and co-morbidity, not about treating, curing, or preventing the disease itself.
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The neuropathological hallmarks of Alzheimer disease (AD) include "positive" lesions such as amyloid plaques and cerebral amyloid angiopathy, neurofibrillary tangles, and glial responses, and "negative" lesions such as neuronal and synaptic loss.
Why it matters
This review of postmortem brain studies describes the hallmark changes of Alzheimer's disease: amyloid plaques, tangles and glial responses, plus loss of neurons and synapses. It reports that amyloid builds up mostly before memory and thinking problems begin, while tangles, neuron loss and "particularly synaptic loss" keep pace with cognitive decline, along a continuum from "normal" aging to dementia; brain imaging in living people has "largely validated" this picture. It summarises the basis for staging and diagnosis and is not a treatment, a test, or proof that amyloid causes the disease.
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These findings suggest that CSF VILIP-1 and VILIP-1/Aβ42 offer diagnostic utility for early AD, and can predict future cognitive impairment in cognitively normal individuals similarly to tau and tau/Aβ42, respectively.
Why it matters
Spinal fluid levels of VILIP-1 distinguished people with Alzheimer disease from cognitively normal people and those with other dementias, and predicted future cognitive impairment in normal individuals. This is a diagnostic and prognostic marker study, not a therapy.
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Why it matters
Describes subtypes of Alzheimer's disease defined by neuropathology that had distinct clinical characteristics, in a retrospective study.
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57/100
Senile plaques are a prominent pathological feature of Alzheimer's disease (AD), but little is understood about the association of glial cells with plaques or about the dynamics of glial responses through the disease course.
Why it matters
In brain tissue examined after death from 91 people with Alzheimer's and 15 without dementia, the amount of amyloid levelled off soon after symptoms began, but reactive astrocytes and microglia (the brain's support and immune cells) kept rising across the illness and tracked tau tangles rather than total amyloid. Glial reactions still grew around existing plaques, so the authors argue against a "straightforward" plaque–glia link and suggest reactive glia "might contribute" to ongoing nerve damage. Each brain was studied once, in one region, so this shows an association across people, not cause and effect, and it tests no treatment.
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The European Union AddNeuroMed program and the US-based Alzheimer Disease Neuroimaging Initiative (ADNI) are two large multi-center initiatives designed to collect and validate biomarker data for Alzheimer's disease (AD).
Why it matters
This study combined MRI data from European and North American cohorts and found similar patterns of brain atrophy, with models predicting conversion from mild cognitive impairment to Alzheimer's disease in about 71% of converters. It concerns imaging classification and prediction, not a treatment, so it does not show how to cure or prevent the disease.
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Asymptomatic Aβ deposition in older adults is strongly associated with LMH.
Why it matters
Lobar microhemorrhages were present in 30.8% of Alzheimer's disease, 35.7% of mild cognitive impairment, and 19.1% of healthy control subjects, and healthy controls with lobar microhemorrhages had significantly higher mean neocortical amyloid binding. Asymptomatic amyloid deposition in older adults was strongly associated with lobar microhemorrhages.
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Disruption of functional connectivity between brain regions may represent an early functional consequence of β-amyloid pathology prior to clinical Alzheimer's disease.
Why it matters
This imaging study found that non-demented people with elevated amyloid had disrupted connectivity in highly connected brain regions, along with reduced metabolism, and that subtle changes were already present in those without symptoms. The authors note these findings were not solely explained by regional atrophy.
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Alzheimer's disease (AD) was first described a little more than 100 years ago.
Why it matters
This review states that there is currently no effective treatment that delays the onset or slows the progression of Alzheimer's disease. It suggests that if the disease is detected before symptoms appear, treatments based on knowledge of its underlying pathogenesis might be effective, but this is a proposal rather than a demonstrated treatment.
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Why it matters
Covers apolipoprotein E in Alzheimer's disease and other neurological disorders.
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The cognitive profile was predominantly amnestic and was associated with multiple domains.
Why it matters
This retrospective cohort study of presenilin 1 E280A familial early-onset Alzheimer's disease reports that the cognitive profile in pre-dementia stages was predominantly amnestic and involved multiple domains. The available text provides no further information on treatment, cure or prevention.
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In older adults, variable agreement between in vivo imaging and CERAD NP score was observed.
Why it matters
In six older adults, amyloid PET imaging during life agreed with autopsy plaque findings when amyloid levels were clearly high or clearly low, but agreement was limited at intermediate levels. This is a small case series comparing an imaging method with autopsy results and does not test any treatment.
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These six markers describe six clinicopathological stages from cognitive normalcy to mild dementia, including stages defined by increased risk of cognitive decline.
Why it matters
Six cerebrospinal fluid proteins were found to distinguish people with mild Alzheimer's dementia from cognitively normal controls, and these markers were applied to a larger independent group that included very mild dementia. This is a biomarker discovery and validation study and does not show that any treatment, cure, or prevention works.
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The study will explore the added value of a multifaceted intervention programme and contribute to the design of future interventions for patients with mild dementia and their caregivers.
Why it matters
This paper describes the design and baseline characteristics of a Danish trial of a counselling and teaching programme for people with mild dementia and their caregivers. No results on whether the intervention works are reported here, so it cannot yet say anything about treating, curing, or preventing Alzheimer's disease.
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Our genome-wide search of Caribbean Hispanic individuals identified several novel genetic variants associated with LOAD and replicated these associations in a white cohort.
Why it matters
This genome-wide study in Caribbean Hispanic individuals identified several genetic variants associated with late-onset Alzheimer's disease and replicated associations for CLU, PICALM, and BIN1. It adds to understanding of genetic risk factors but does not provide a treatment, cure, or prevention.
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Three decades of genetic research in Alzheimer disease (AD) have substantially broadened our understanding of the pathogenetic mechanisms leading to neurodegeneration and dementia.
Why it matters
This review notes that known disease genes still leave much of Alzheimer's heritability unexplained, and that rare sequence variants may account for this missing heritability. It is a review of genetics and does not report a treatment, cure, or prevention.
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In a community-dwelling population with generally mild AD, hospitalization is frequent, occurring in two-thirds of participants over a median follow-up time of 3 years.
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The molecular pathways leading to Alzheimer-type dementia are not well understood, but the amyloid beta-protein is believed to be centrally involved.
Why it matters
In this study of 43 brains, amyloid beta-protein monomer in certain extracts was strongly associated with Alzheimer-type dementia, and a sodium dodecyl sulphate-stable amyloid beta-protein dimer was detected specifically and sensitively in extracts from dementia cases. The findings suggest that soluble non-plaque forms of amyloid beta-protein, rather than plaque quantity, relate to clinical status.
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.
- Alzheimer Disease Biomarkers and Subjective Cognitive Decline Among Hispanic and/or Latino Adults
- Application of Convolutional Neural Network Based on ResNet18 for Alzheimer Disease Classification
- Adjuvant transcranial direct current stimulation for treating Alzheimer's disease: A case study
- Diagnostic performance of plasma GFAP in preclinical stages of Alzheimer's disease using the Lumipulse platform
- Could a Mediterranean Diet Modulate Alzheimer’s Disease Progression? The Role of Gut Microbiota and Metabolite Signatures in Neurodegeneration
- Rural-Urban Differences in Alzheimer's Disease and Related Disorders Diagnostic Prevalence in Kentucky and West Virginia
- Time course of the development of Alzheimer-like pathology in the doubly transgenic PS1+APP mouse
- In vivo imaging of amyloid deposition in Alzheimer disease using the radioligand 18F-AV-45 (florbetapir [corrected] F 18)
- Neurofibrillary tangles mediate the association of amyloid load with clinical Alzheimer disease and level of cognitive function
- Role of protein kinase B in Alzheimer's neurofibrillary pathology