Apolipoprotein E: Structure and Function in Lipid Metabolism, Neurobiology, and Alzheimer’s Diseases
By Yadong Huang, R. Mahley. Neurobiology of Disease, 2014
720 citations recorded by the source corpus.
Apolipoprotein (apo) E is a multifunctional protein with central roles in lipid metabolism, neurobiology, and neurodegenerative diseases. It has three major isoforms (apoE2, apoE3, and apoE4) with different effects on lipid and neuronal homeostasis. A major function of apoE is to mediate the binding of lipoproteins or lipid complexes in the plasma or interstitial fluids to specific cell-surface receptors. These receptors internalize apoE-containing lipoprotein particles; thus, apoE participates in the distribution/redistribution of lipids among various tissues and cells of the body. In addition, intracellular apoE may modulate various cellular processes physiologically or pathophysiologically, including cytoskeletal assembly and stability, mitochondrial integrity and function, and dendritic morphology and function. Elucidation of the functional domains within this protein and of the three-dimensional structure of the major isoforms of apoE has contributed significantly to our understanding of its physiological and pathophysiological roles at a molecular level. It is likely that apoE, with its multiple cellular origins and multiple structural and biophysical properties, is involved widely in processes of lipid metabolism and neurobiology, possibly encompassing a variety of disorders of neuronal repair, remodeling, and degeneration by interacting with different factors through various pathways.
Subfields: Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/ade0e34b03eac43726ea64dfae318fa9a5825836
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Citations in the corpus
- Alzheimer’s disease: experimental models and reality (2017, background): “The strongest identified genetic risk factor for sAD is the inheritance of the apolipoprotein (apo) E4 allele, the protein product of which influences the aggregation and clearance of brain Aβ [63, 115].”
- The amyloid hypothesis of Alzheimer's disease at 25 years (2016, background): “Other potential mechanisms have been suggested, including an adverse effect of ApoE4 on the processing of tau in neurons (Andrews-Zwilling et al, 2010; Huang & Mahley, 2014).”
- Impact of multiple pathologies on the threshold for clinically overt dementia (2017, background): “, apoE e4 is related to risk of amyloid deposition, CAA, LB and to a lesser degree cerebral infarcts [47]); and inflammatory mechanisms may be a mechanism of injury in multiple neurodegenerative and vascular diseases.”