Literature DB >> 32753441

Limbic-predominant age-related TDP-43 encephalopathy, ADNC pathology, and cognitive decline in aging.

Alifiya Kapasi1, Lei Yu2, Patricia A Boyle2, Lisa L Barnes2, David A Bennett2, Julie A Schneider2.   

Abstract

OBJECTIVE: To examine the impact of 3 pathologic groups, pure limbic-predominant age-related transactive response DNA-binding protein 43 encephalopathy (LATE) neuropathologic changes (NC), pure Alzheimer disease neuropathologic change (ADNC), and mixed ADNC with LATE-NC, on late-life cognitive decline.
METHODS: Data came from 1,356 community-based older persons who completed detailed annual cognitive testing and systematic neuropathologic examination at autopsy to identify LATE-NC, ADNC, and other age-related pathologies. Persons were categorized into (0) a group without a pathologic diagnosis of LATE or ADNC (n = 378), (1) LATE-NC without ADNC (n = 91), (2) ADNC without LATE-NC (n = 535), and (3) mixed ADNC with LATE-NC (n = 352). We used mixed-effect models to examine the group associations with rate of decline in global cognition and 5 cognitive domains and then examined whether age modified associations.
RESULTS: Compared to those without LATE-NC or ADNC, those with pure LATE-NC had a faster decline in global cognition (p = 0.025) and episodic memory (p = 0.002); however, compared to persons with pure ADNC, those with pure LATE-NC showed a slower decline. Those with mixed ADNC with LATE-NC showed the fastest decline compared to those with either pathology alone. Persons ≥90 years of age with mixed ADNC with LATE-NC had slower cognitive decline compared to those ≤89 years of age.
CONCLUSION: Persons with pure LATE-NC follow a slower trajectory compared to those with pure ADNC. Those with mixed LATE/ADNC have a steeper decline than individuals with either pathology alone. In addition, age may modify the effect of pathology on cognitive decline. These findings have important implications for the development of biomarkers and prognosis for late-life cognitive decline. CLASSIFICATION OF EVIDENCE: This study provides Class I evidence that LATE-NC and Alzheimer disease pathologic changes are associated with different trajectories of late-life cognitive decline.
© 2020 American Academy of Neurology.

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Year:  2020        PMID: 32753441      PMCID: PMC7682843          DOI: 10.1212/WNL.0000000000010454

Source DB:  PubMed          Journal:  Neurology        ISSN: 0028-3878            Impact factor:   9.910


  36 in total

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2.  Overlapping but distinct TDP-43 and tau pathologic patterns in aged hippocampi.

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3.  Neurodegenerative disease concomitant proteinopathies are prevalent, age-related and APOE4-associated.

Authors:  John L Robinson; Edward B Lee; Sharon X Xie; Lior Rennert; EunRan Suh; Colin Bredenberg; Carrie Caswell; Vivianna M Van Deerlin; Ning Yan; Ahmed Yousef; Howard I Hurtig; Andrew Siderowf; Murray Grossman; Corey T McMillan; Bruce Miller; John E Duda; David J Irwin; David Wolk; Lauren Elman; Leo McCluskey; Alice Chen-Plotkin; Daniel Weintraub; Steven E Arnold; Johannes Brettschneider; Virginia M-Y Lee; John Q Trojanowski
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4.  TDP-43 stage, mixed pathologies, and clinical Alzheimer's-type dementia.

Authors:  Bryan D James; Robert S Wilson; Patricia A Boyle; John Q Trojanowski; David A Bennett; Julie A Schneider
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5.  Depressive symptoms, cognitive decline, and risk of AD in older persons.

Authors:  Robert S Wilson; L L Barnes; C F Mendes de Leon; N T Aggarwal; J S Schneider; J Bach; J Pilat; L A Beckett; S E Arnold; D A Evans; D A Bennett
Journal:  Neurology       Date:  2002-08-13       Impact factor: 9.910

6.  Cerebral infarctions and the likelihood of dementia from Alzheimer disease pathology.

Authors:  J A Schneider; R S Wilson; J L Bienias; D A Evans; D A Bennett
Journal:  Neurology       Date:  2004-04-13       Impact factor: 9.910

7.  Temporal course of neurodegenerative effects on cognition in old age.

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Review 8.  Religious Orders Study and Rush Memory and Aging Project.

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9.  Hippocampal sclerosis of aging is a key Alzheimer's disease mimic: clinical-pathologic correlations and comparisons with both alzheimer's disease and non-tauopathic frontotemporal lobar degeneration.

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10.  Limbic-predominant age-related TDP-43 encephalopathy (LATE): consensus working group report.

Authors:  Peter T Nelson; Dennis W Dickson; John Q Trojanowski; Clifford R Jack; Patricia A Boyle; Konstantinos Arfanakis; Rosa Rademakers; Irina Alafuzoff; Johannes Attems; Carol Brayne; Ian T S Coyle-Gilchrist; Helena C Chui; David W Fardo; Margaret E Flanagan; Glenda Halliday; Suvi R K Hokkanen; Sally Hunter; Gregory A Jicha; Yuriko Katsumata; Claudia H Kawas; C Dirk Keene; Gabor G Kovacs; Walter A Kukull; Allan I Levey; Nazanin Makkinejad; Thomas J Montine; Shigeo Murayama; Melissa E Murray; Sukriti Nag; Robert A Rissman; William W Seeley; Reisa A Sperling; Charles L White; Lei Yu; Julie A Schneider
Journal:  Brain       Date:  2019-06-01       Impact factor: 15.255

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  13 in total

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Review 2.  Limbic-Predominant Age-Related TDP-43 Encephalopathy: LATE-Breaking Updates in Clinicopathologic Features and Biomarkers.

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4.  TDP-43 Pathology Exacerbates Cognitive Decline in Primary Age-Related Tauopathy.

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6.  Neuropathological associations of limbic-predominant age-related TDP-43 encephalopathy neuropathological change (LATE-NC) differ between the oldest-old and younger-old.

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Journal:  Nat Rev Neurol       Date:  2022-03-24       Impact factor: 44.711

8.  Coping with brain amyloid: genetic heterogeneity and cognitive resilience to Alzheimer's pathophysiology.

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9.  TDP-43 promotes tau accumulation and selective neurotoxicity in bigenic Caenorhabditis elegans.

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10.  Lower White Matter Volume and Worse Executive Functioning Reflected in Higher Levels of Plasma GFAP among Older Adults with and Without Cognitive Impairment.

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Journal:  J Int Neuropsychol Soc       Date:  2021-06-22       Impact factor: 3.114

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