The cell biology of APOE in the brain
IA Windham, S Cohen - Trends in cell biology, 2024 - cell.com
Apolipoprotein E (APOE) traffics lipids in the central nervous system. The E4 variant of APOE
is a major genetic risk factor for Alzheimer's disease (AD) and a multitude of other …
is a major genetic risk factor for Alzheimer's disease (AD) and a multitude of other …
[HTML][HTML] ApoE Cascade Hypothesis in the pathogenesis of Alzheimer's disease and related dementias
The ε4 allele of the apolipoprotein E gene (APOE4) is a strong genetic risk factor for
Alzheimer's disease (AD) and several other neurodegenerative conditions, including Lewy …
Alzheimer's disease (AD) and several other neurodegenerative conditions, including Lewy …
APOE from astrocytes restores Alzheimer's Aβ-pathology and DAM-like responses in APOE deficient microglia
P Preman, D Moechars, E Fertan, L Wolfs… - EMBO Molecular …, 2024 - embopress.org
The major genetic risk factor for Alzheimer's disease (AD), APOE4, accelerates beta-amyloid
(Aβ) plaque formation, but whether this is caused by APOE expressed in microglia or …
(Aβ) plaque formation, but whether this is caused by APOE expressed in microglia or …
ApoE4 expression disrupts tau uptake, trafficking, and clearance in astrocytes
M Eisenbaum, A Pearson, C Ortiz, M Mullan… - Glia, 2024 - Wiley Online Library
Tauopathies are a collection of neurodegenerative diseases characterized by the
accumulation of pathogenic aggregates of the microtubule‐associated protein tau. Despite …
accumulation of pathogenic aggregates of the microtubule‐associated protein tau. Despite …
Early lysosome defects precede neurodegeneration with amyloid-β and tau aggregation in NHE6-null rat brain
Loss-of-function mutations in the X-linked endosomal Na+/H+ exchanger 6 (NHE6) cause
Christianson syndrome in males. Christianson syndrome involves endosome dysfunction …
Christianson syndrome in males. Christianson syndrome involves endosome dysfunction …
A multi‐hit hypothesis for an APOE4‐dependent pathophysiological state
The APOE gene encoding the Apolipoprotein E protein is the single most significant genetic
risk factor for late‐onset Alzheimer's disease. The APOE4 genotype confers a significantly …
risk factor for late‐onset Alzheimer's disease. The APOE4 genotype confers a significantly …
Cell type-specific functions of Alzheimer's disease endocytic risk genes
JK Maninger, K Nowak… - … of the Royal …, 2024 - royalsocietypublishing.org
Endocytosis is a key cellular pathway required for the internalization of cellular nutrients,
lipids and receptor-bound cargoes. It is also critical for the recycling of cellular components …
lipids and receptor-bound cargoes. It is also critical for the recycling of cellular components …
[HTML][HTML] Loss of endosomal exchanger NHE6 leads to pathological changes in tau in human neurons
MA Fernandez, F Bah, L Ma, YJ Lee, M Schmidt… - Stem Cell Reports, 2022 - cell.com
Disruption of endolysosomal and autophagy-lysosomal systems is increasingly implicated in
neurodegeneration. Sodium-proton exchanger 6 (NHE6) contributes to the maintenance of …
neurodegeneration. Sodium-proton exchanger 6 (NHE6) contributes to the maintenance of …
Report of the APOE4 National Institute on Aging/Alzheimer Disease Sequencing Project Consortium Working Group: Reducing APOE4 in Carriers is a Therapeutic …
Alzheimer's disease (AD) is the most common neurodegenerative disorder and one of the
leading causes of disability worldwide. The apolipoprotein E4 gene (APOE4) is the strongest …
leading causes of disability worldwide. The apolipoprotein E4 gene (APOE4) is the strongest …
Circadian Regulation of Apolipoproteins in the Brain: Implications in Lipid Metabolism and Disease
CH Lee, CE Murrell, A Chu, X Pan - International Journal of Molecular …, 2023 - mdpi.com
The circadian rhythm is a 24 h internal clock within the body that regulates various factors,
including sleep, body temperature, and hormone secretion. Circadian rhythm disruption is …
including sleep, body temperature, and hormone secretion. Circadian rhythm disruption is …