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8 sty 2024 · The ɛ4 allele of the apolipoprotein E gene (APOE), which translates to the APOE4 isoform, is the strongest genetic risk factor for late-onset Alzheimer disease (AD). Within the CNS, APOE is...
- Apolipoprotein E in Alzheimer’s disease trajectories and the next ...
Alzheimer’s disease (AD) is a complex, progressive primary...
- A cell-autonomous role for border-associated macrophages in ApoE4 ...
We report that in ApoE4 mice perivascular macrophages are...
- Apolipoprotein E in Alzheimer’s disease trajectories and the next ...
19 cze 2024 · Alzheimer’s disease (AD) is a complex, progressive primary neurodegenerative disease. Since pivotal genetic studies in 1993, the ε4 allele of the apolipoprotein E gene (APOE ε4) has remained the...
18 wrz 2024 · We report that in ApoE4 mice perivascular macrophages are the sole source and effectors of the ApoE4 mediating the neurovascular dysfunction, enhanced white matter damage and cognitive...
Tematy dnia
30 paź 2024 · Background: Apolipoprotein E (APOE = gene, ApoE = protein) is a glycoprotein involved in the biological process of lipid transportation and metabolism, contributing to lipid homeostasis. APOE has been extensively studied for its correlation with neurodegenerative diseases, in particular Alzheimer’s disease (AD), where the possession of the epsilon 4 (E4) allele is established as a risk ...
Therefore, another potential treatment is to disrupt this ApoE4 domain interaction with a “structural corrector” and treat ApoE4-expressing Neuro-2a cells with this structural corrector to make the protein more “ApoE3-like” in structure and function (Huang and Mahley, 2014). Other effective small molecules that inhibit interdomain ...
The ɛ4 allele of the apolipoprotein E gene (APOE) is the strongest genetic risk factor for late-onset Alzheimer disease (AD). Within the CNS, APOE is produced by a variety of cell types under different conditions, posing a challenge for studying its roles in AD pathogenesis.
Here, we review these scientific advances and propose a cell type-specific APOE4 cascade model of AD. In this model, neuronal APOE4 emerges as a crucial pathological initiator and driver of AD pathogenesis, instigating glial responses and, ultimately, neurodegeneration.
