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Shi et al. determined that ApoE4 exacerbates tau-mediated neurodegeneration, independently of amyloid-β pathology, while the lack of ApoE protects against pathology. In support, compared to ApoE3- and ApoE2-expressing mice, ApoE4-expressing mice demonstrated significantly increased volume of the lateral ventricle, concomitant with the loss of tissue in the piriform cortex, hippocampus and loss of the granule layer of the dentate gyrus. Moreover, microglia and astrocytes isolated from ApoE4-expressing mice exhibited a marked upregulation in proinflammatory genes, which contributes to neuroinflammation and neurodegeneration. Most importantly, in vitro treatment of P301S tau-expressing neurons with recombinant ApoE alone led to increased neuronal death and these effects were most prominent when neurons were treated with ApoE4. This data suggests a direct effect of ApoE4 on neurodegeneration. In sum, the authors propose that under pathological tau accumulation, ApoE, and specifically ApoE4, exacerbates neurodegeneration, whereas lack of ApoE dampens neurodegeneration. Dying neurons promote neuroinflammation, which is further amplified by ApoE4 owing to its increased innate immune reactivity, aggravating neurodegeneration further.
 

Adapted from Shi, et al. 2017. Nature. 549, 523–527. Pubmed

Shi et al. determined that ApoE4 exacerbates tau-mediated neurodegeneration, independently of amyloid-β pathology, while the lack of ApoE protects against pathology. In support, compared to ApoE3- and ApoE2-expressing mice, ApoE4-expressing mice demonstrated significantly increased volume of the lateral ventricle, concomitant with the loss of tissue in the piriform cortex, hippocampus and loss of the granule layer of the dentate gyrus. Moreover, microglia and astrocytes isolated from ApoE4-expressing mice exhibited a marked upregulation in proinflammatory genes, which contributes to neuroinflammation and neurodegeneration. Most importantly, in vitro treatment of P301S tau-expressing neurons with recombinant ApoE alone led to increased neuronal death and these effects were most prominent when neurons were treated with ApoE4. This data suggests a direct effect of ApoE4 on neurodegeneration. In sum, the authors propose that under pathological tau accumulation, ApoE, and specifically ApoE4, exacerbates neurodegeneration, whereas lack of ApoE dampens neurodegeneration. Dying neurons promote neuroinflammation, which is further amplified by ApoE4 owing to its increased innate immune reactivity, aggravating neurodegeneration further .

BioLegend offers several antibodies to detect ApoE and tau isoforms by WB, ELISA and IHC. In addition, we provide a LEGENDplex™ Human Apo Panel that can assess the relative concentration of human Apolipoproteins, including ApoE4, in serum, plasma and cell culture supernatant samples.

Strong staining of ApoE4-containing plaques on formalin fixed paraffin embedded human Alzheimer’s brain tissue using Clone 5A9 (Cat. No. 811701) at 4 µg/mL.