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. 2023 Oct;18(10):2200-2201.
doi: 10.4103/1673-5374.367841.

Reevaluating the cause of laminopathy in Alzheimer's disease

Md Imamul Islam  1 , Eftekhar Eftekharpour  1
Affiliations

Reevaluating the cause of laminopathy in Alzheimer's disease

Md Imamul Islam et al. Neural Regen Res. 2023 Oct.
No abstract available

PubMed Disclaimer

Conflict of interest statement

None

Figures

Figure 1
Figure 1
Schematic illustration of laminopathy and histone modifications induced by Aβ42 and Trx1 oxidation. (1, 2, 3) Aβ42 induces endoplasmic reticulum stress and lysosomal membrane permeabilization activating CTSL which cleaves LB1 and induces histone modifications. The gene expression pattern resulted from histone modifications requires further studies. CTSL inhibits caspase-6 mediated LB1 cleavage by degrading caspase-6. Oxidation/inhibition of Trx1 activates caspase-6 and initiates LB1 cleavage and downstream changes. Aβ42: Amyloid-beta 42; CTSL: cathepsin L; ER: endoplasmic reticulum; LB1: lamin B1; Trx1: thioredoxin-1. Created with BioRender.com.
See this image and copyright information in PMC

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