Papers published on a yearly basis
Papers
More filters
••
Johns Hopkins University School of Medicine1, Johns Hopkins University2, Mayo Clinic3, McGill University4, Harvard University5, University of California, Irvine6, University of Pittsburgh7, Columbia University Medical Center8, Eli Lilly and Company9, Washington University in St. Louis10, UCL Institute of Neurology11, VU University Medical Center12, Alzheimer's Association13, Northwestern University14, National Institutes of Health15
TL;DR: The workgroup sought to ensure that the revised criteria would be flexible enough to be used by both general healthcare providers without access to neuropsychological testing, advanced imaging, and cerebrospinal fluid measures, and specialized investigators involved in research or in clinical trial studies who would have these tools available.
Abstract: The National Institute on Aging and the Alzheimer's Association charged a workgroup with the task of revising the 1984 criteria for Alzheimer's disease (AD) dementia. The workgroup sought to ensure that the revised criteria would be flexible enough to be used by both general healthcare providers without access to neuropsychological testing, advanced imaging, and cerebrospinal fluid measures, and specialized investigators involved in research or in clinical trial studies who would have these tools available. We present criteria for all-cause dementia and for AD dementia. We retained the general framework of probable AD dementia from the 1984 criteria. On the basis of the past 27 years of experience, we made several changes in the clinical criteria for the diagnosis. We also retained the term possible AD dementia, but redefined it in a manner more focused than before. Biomarker evidence was also integrated into the diagnostic formulations for probable and possible AD dementia for use in research settings. The core clinical criteria for AD dementia will continue to be the cornerstone of the diagnosis in clinical practice, but biomarker evidence is expected to enhance the pathophysiological specificity of the diagnosis of AD dementia. Much work lies ahead for validating the biomarker diagnosis of AD dementia.
13,710 citations
••
TL;DR: A useful conceptual framework is provided for matching the functional imaging findings with the specific role(s) played by this structure in the higher-order cognitive functions in which it has been implicated, and activation patterns appear to converge with anatomical and connectivity data in providing preliminary evidence for a functional subdivision within the precuneus.
Abstract: Functional neuroimaging studies have started unravelling unexpected functional attributes for the posteromedial portion of the parietal lobe, the precuneus. This cortical area has traditionally received little attention, mainly because of its hidden location and the virtual absence of focal lesion studies. However, recent functional imaging findings in healthy subjects suggest a central role for the precuneus in a wide spectrum of highly integrated tasks, including visuo-spatial imagery, episodic memory retrieval and self-processing operations, namely first-person perspective taking and an experience of agency. Furthermore, precuneus and surrounding posteromedial areas are amongst the brain structures displaying the highest resting metabolic rates (hot spots) and are characterized by transient decreases in the tonic activity during engagement in non-self-referential goal-directed actions (default mode of brain function). Therefore, it has recently been proposed that precuneus is involved in the interwoven network of the neural correlates of self-consciousness, engaged in self-related mental representations during rest. This hypothesis is consistent with the selective hypometabolism in the posteromedial cortex reported in a wide range of altered conscious states, such as sleep, drug-induced anaesthesia and vegetative states. This review summarizes the current knowledge about the macroscopic and microscopic anatomy of precuneus, together with its wide-spread connectivity with both cortical and subcortical structures, as shown by connectional and neurophysiological findings in non-human primates, and links these notions with the multifaceted spectrum of its behavioural correlates. By means of a critical analysis of precuneus activation patterns in response to different mental tasks, this paper provides a useful conceptual framework for matching the functional imaging findings with the specific role(s) played by this structure in the higher-order cognitive functions in which it has been implicated. Specifically, activation patterns appear to converge with anatomical and connectivity data in providing preliminary evidence for a functional subdivision within the precuneus into an anterior region, involved in self-centred mental imagery strategies, and a posterior region, subserving successful episodic memory retrieval.
4,342 citations
••
TL;DR: In a recent study, this article showed that low cerebrospinal fluid (CSF) Aβ42 and amyloid-PET positivity precede other AD manifestations by many years.
Abstract: Despite continuing debate about the amyloid β‐protein (or Aβ hypothesis, new lines of evidence from laboratories and clinics worldwide support the concept that an imbalance between production and clearance of Aβ42 and related Aβ peptides is a very early, often initiating factor in Alzheimer9s disease (AD). Confirmation that presenilin is the catalytic site of γ‐secretase has provided a linchpin: all dominant mutations causing early‐onset AD occur either in the substrate (amyloid precursor protein, APP) or the protease (presenilin) of the reaction that generates Aβ. Duplication of the wild‐type APP gene in Down9s syndrome leads to Aβ deposits in the teens, followed by microgliosis, astrocytosis, and neurofibrillary tangles typical of AD. Apolipoprotein E4, which predisposes to AD in > 40% of cases, has been found to impair Aβ clearance from the brain. Soluble oligomers of Aβ42 isolated from AD patients9 brains can decrease synapse number, inhibit long‐term potentiation, and enhance long‐term synaptic depression in rodent hippocampus, and injecting them into healthy rats impairs memory. The human oligomers also induce hyperphosphorylation of tau at AD‐relevant epitopes and cause neuritic dystrophy in cultured neurons. Crossing human APP with human tau transgenic mice enhances tau‐positive neurotoxicity. In humans, new studies show that low cerebrospinal fluid (CSF) Aβ42 and amyloid‐PET positivity precede other AD manifestations by many years. Most importantly, recent trials of three different Aβ antibodies (solanezumab, crenezumab, and aducanumab) have suggested a slowing of cognitive decline in post hoc analyses of mild AD subjects. Although many factors contribute to AD pathogenesis, Aβ dyshomeostasis has emerged as the most extensively validated and compelling therapeutic target.
3,824 citations
••
Cardiff University1, Medical Research Council2, University of Bristol3, National Institute for Health Research4, King's College5, Trinity College, Dublin6, University of Cambridge7, University of Nottingham8, Queen's University Belfast9, University of Southampton10, University of Manchester11, John Radcliffe Hospital12, UCL Institute of Neurology13, University of Bonn14, University of Hamburg15, Charité16, University of Erlangen-Nuremberg17, University of Duisburg-Essen18, Ludwig Maximilian University of Munich19, Heidelberg University20, University College Dublin21, University of Freiburg22, Washington University in St. Louis23, Brigham Young University24, University of Antwerp25, University College London26, Wellcome Trust Sanger Institute27, King's College London28, Aristotle University of Thessaloniki29, National Institutes of Health30, Mayo Clinic31
TL;DR: A two-stage genome-wide association study of Alzheimer's disease involving over 16,000 individuals, the most powerful AD GWAS to date, produced compelling evidence for association with Alzheimer's Disease in the combined dataset.
Abstract: We undertook a two-stage genome-wide association study (GWAS) of Alzheimer's disease (AD) involving over 16,000 individuals, the most powerful AD GWAS to date. In stage 1 (3,941 cases and 7,848 controls), we replicated the established association with the apolipoprotein E (APOE) locus (most significant SNP, rs2075650, P = 1.8 10-157) and observed genome-wide significant association with SNPs at two loci not previously associated with the disease: at the CLU (also known as APOJ) gene (rs11136000, P = 1.4 10-9) and 5' to the PICALM gene (rs3851179, P = 1.9 10-8). These associations were replicated in stage 2 (2,023 cases and 2,340 controls), producing compelling evidence for association with Alzheimer's disease in the combined dataset (rs11136000, P = 8.5 10-10, odds ratio = 0.86; rs3851179, P = 1.3 10-9, odds ratio = 0.86).
2,956 citations
••
TL;DR: NODDI provides sensible neurite density and orientation dispersion estimates, thereby disentangling two key contributing factors to FA and enabling the analysis of each factor individually, and demonstrates the feasibility of NODDI even for the most time-sensitive clinical applications, such as neonatal and dementia imaging.
2,354 citations
Authors
Showing all 3663 results
Name | H-index | Papers | Citations |
---|---|---|---|
Karl J. Friston | 217 | 1267 | 217169 |
David Miller | 203 | 2573 | 204840 |
Mark I. McCarthy | 200 | 1028 | 187898 |
Raymond J. Dolan | 196 | 919 | 138540 |
Paul M. Thompson | 183 | 2271 | 146736 |
David R. Williams | 178 | 2034 | 138789 |
John Hardy | 177 | 1178 | 171694 |
Chris D. Frith | 173 | 524 | 130472 |
David Baker | 173 | 1226 | 109377 |
Kaj Blennow | 160 | 1845 | 116237 |
Frederik Barkhof | 154 | 1449 | 104982 |
David J. Brooks | 152 | 1056 | 94335 |
Marvin Johnson | 149 | 1827 | 119520 |
Walter Paulus | 149 | 809 | 86252 |
Richard S. J. Frackowiak | 142 | 309 | 100726 |