Regarding the possible pathogenic relevance of TNIs, lamin dysfunction and neuronal nuclear indentations in AD have been linked to the improper cytoskeletal/nucleoskeletal coupling that was suggested as a novel mediator of neurotoxicity in Tauopathies (Frost et al., 2016) and more recently, pathological Tau has been shown to impair nucleocytoplasmic transport in Tau-overexpressing mice and AD brain tissue (Eftekharzadeh et al., 2018) which has been further confirmed recently (Paonessa et al., 2019). This evidence concerns the gene LMNA and Alzheimer disease.