Mild cognitive impairment with suspected nonamyloid pathology (SNAP): Prediction of progression - Wikidata - wikimedia - TriplyDB

Mild cognitive impairment with suspected nonamyloid pathology (SNAP): Prediction of progression

Mild cognitive impairment with suspected nonamyloid pathology (SNAP): Prediction of progression

http://www.wikidata.org/entity/Q35106472

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Unified theory of Alzheimer's disease (UTAD): implications for prevention and curative therapy Suspected non-Alzheimer disease pathophysiology--concept and controversy Magnetic resonance imaging in Alzheimer's Disease Neuroimaging Initiative 2 Evolving Evidence for the Value of Neuroimaging Methods and Biological Markers in Subjects Categorized with Subjective Cognitive Decline.Future Directions in Imaging Neurodegeneration.Communicating mild cognitive impairment diagnoses with and without amyloid imaging.Mapping 3-year changes in gray matter and metabolism in Aβ-positive nondemented subjects.Different definitions of neurodegeneration produce similar amyloid/neurodegeneration biomarker group findings Role of β-Amyloidosis and Neurodegeneration in Subsequent Imaging Changes in Mild Cognitive Impairment Hippocampal and Clinical Trajectories of Mild Cognitive Impairment with Suspected Non-Alzheimer's Disease Pathology.Age-specific and sex-specific prevalence of cerebral β-amyloidosis, tauopathy, and neurodegeneration in cognitively unimpaired individuals aged 50-95 years: a cross-sectional study.Alzheimer Disease Signature Neurodegeneration and APOE Genotype in Mild Cognitive Impairment With Suspected Non-Alzheimer Disease Pathophysiology.Patient and caregiver reactions to clinical amyloid imaging.Added value and limitations of amyloid-PET imaging: review and analysis of selected cases of mild cognitive impairment and dementia.Therapeutic efficacy of the Ginkgo special extract EGb761® within the framework of the mitochondrial cascade hypothesis of Alzheimer's disease.Longitudinal β-Amyloid Deposition and Hippocampal Volume in Preclinical Alzheimer Disease and Suspected Non-Alzheimer Disease Pathophysiology.Evolution of neurodegeneration-imaging biomarkers from clinically normal to dementia in the Alzheimer disease spectrum.Biomarkers in subtypes of mild cognitive impairment and subjective cognitive decline.NIA-AA staging of preclinical Alzheimer disease: discordance and concordance of CSF and imaging biomarkers.Phase II clinical trials of anti-amyloid β antibodies: When is enough, enough?APOE allele frequencies in suspected non-amyloid pathophysiology (SNAP) and the prodromal stages of Alzheimer's Disease.Cerebrospinal fluid and blood biomarkers for neurodegenerative dementias: An update of the Consensus of the Task Force on Biological Markers in Psychiatry of the World Federation of Societies of Biological Psychiatry.The Effects of Cortical Hypometabolism and Hippocampal Atrophy on Clinical Trajectories in Mild Cognitive Impairment with Suspected Non-Alzheimer's Pathology: A Brief Report.Weighting and standardization of frequencies to determine prevalence of AD imaging biomarkers.Amyloid β Deposition and Suspected Non-Alzheimer Pathophysiology and Cognitive Decline Patterns for 12 Years in Oldest Old Participants Without Dementia.A Cochrane review on brain [¹⁸F]FDG PET in dementia: limitations and future perspectives.Decreased hippocampal metabolism in high-amyloid mild cognitive impairment.Patients with Amyloid-Negative Mild Cognitive Impairment have Cortical Hypometabolism but the Hippocampus is Preserved.Diagnostic and Prognostic Value of the Combination of Two Measures of Verbal Memory in Mild Cognitive Impairment due to Alzheimer's Disease.Defining SNAP by cross-sectional and longitudinal definitions of neurodegeneration.Joint associations of β-amyloidosis and cortical thickness with cognition.Association of Neuropathological Markers in the Parietal Cortex With Antemortem Cognitive Function in Persons With Mild Cognitive Impairment and Alzheimer Disease.Addition of the Aβ42/40 ratio to the cerebrospinal fluid biomarker profile increases the predictive value for underlying Alzheimer's disease dementia in mild cognitive impairment.Alzheimer's Disease FDG PET Imaging Pattern in an Amyloid-Negative Mild Cognitive Impairment Subject.NIA-AA Research Framework: Toward a biological definition of Alzheimer's disease.Longitudinal outcomes of amyloid positive versus negative amnestic mild cognitive impairments: a three-year longitudinal study.A biomarker study in long-lasting amnestic mild cognitive impairment.Asymmetry of Hippocampus and Amygdala Defect in Subjective Cognitive Decline Among the Community Dwelling Chinese.

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Mild cognitive impairment with suspected nonamyloid pathology (SNAP): Prediction of progression

http://www.wikidata.org/entity/Q35106472

description

2015 nî lūn-bûn

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2015 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2015 թվականի հունվարին հրատարակված գիտական հոդված

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2015年の論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年论文

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Mild cognitive impairment with ...... AP): Prediction of progression

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Mild cognitive impairment with ...... AP): Prediction of progression

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Anders E Wall

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Anna Caroli

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Annapaola Prestia

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Bart Van Berckel

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Il Han Choo

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Toward defining the preclinical stages of Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease

Mild cognitive impairment: clinical characterization and outcome

Hypothetical model of dynamic biomarkers of the Alzheimer's pathological cascade

Clinical and biomarker changes in dominantly inherited Alzheimer's disease.

Diagnostic accuracy of markers for prodromal Alzheimer's disease in independent clinical series.

Accuracy of the clinical diagnosis of Alzheimer disease at National Institute on Aging Alzheimer Disease Centers, 2005-2010.

Brain imaging and fluid biomarker analysis in young adults at genetic risk for autosomal dominant Alzheimer's disease in the presenilin 1 E280A kindred: a case-control study.

Short-term clinical outcomes for stages of NIA-AA preclinical Alzheimer disease.

Fluid biomarkers in Alzheimer disease.

Apolipoprotein E, not fibrillar β-amyloid, reduces cerebral glucose metabolism in normal aging.

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84

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Philip Scheltens

Giovanni B. Frisoni

Samantha Galluzzi

Michael Schöll

Frederik Barkhof

Alexander Drzezga

Alzheimer's Disease Neuroimaging Initiative

Charlotte Teunissen

Alberto Redolfi

Stephen F Carter

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