13 results for “late-nc”. Showing 13 of 39,449.
Pure LATE-NC: Frequency, clinical impact, and the importance of considering APOE genotype when assessing this and other subtypes of non-Alzheimer's pathologies.
LATE-NC stages). Pure LATE-NC was not associated with
TDP-43 pathology is associated with increased tau burdens and seeding.
LATE-NC, AD(LATE-NC+), have increased burdens of pretangles
10.1093/brain/awz099
LATE-NC. For routine autopsy workup of LATE-NC, an anatomically
Clinical criteria for limbic-predominant age-related TDP-43 encephalopathy.
LATE-NC) is highly prevalent in late life and a common
Limbic-predominant age-related TDP-43 encephalopathy (LATE-NC): Co-pathologies and genetic risk factors provide clues about pathogenesis.
LATE-NC is not rare, LATE-NC often coexists in the same
Alzheimer's disease and its co-pathologies: Implications for hippocampal degeneration, cognitive decline, and the role of APOE ε4.
LATE-NC), α-synuclein, other age-related lesions, and apolipoprotein
Data-driven neuropathological staging and subtyping of TDP-43 proteinopathies.
LATE-NC) with and without Alzheimer's disease (n = 304). The data
Limbic-predominant age-related TDP43 encephalopathy (LATE) neuropathological change in neurodegenerative diseases.
LATE-NC and in LATE-NC associated with coexisting pathologies
Annexin A11 aggregation in FTLD-TDP type C and related neurodegenerative disease proteinopathies.
LATE-NC). Annexin A11 is also known to form aggregates
Alzheimer's disease clinical variants show distinct neuroinflammatory profiles with neuropathology.
LATE-NC), and vascular pathology. For quantitative assessment, we analysed
Hypothesis-based investigation of known AD risk variants reveals the genetic underpinnings of neuropathological lesions observed in Alzheimer's-type dementia.
LATE-NC risk. Furthermore, we identified new putative LATE-NC
Context-dependent Interactors Regulate TDP-43 Dysfunction in ALS/FTLD.
LATE-NC. However, the mechanisms underlying TDP-43 dysfunction remain
A familial missense variant in the Alzheimer's disease gene SORL1 impairs its maturation and endosomal sorting.
LATE-NC). We further characterized this variant and show that