TPPP/p25 has been recognized as a MAP that displays two crucial features: i) it does not have a 3D structure, namely it is disordered2614; ii) it is enriched in inclusions of the neurons and oligodendrocytes in the cases of Parkinson’s disease and multiple system atrophy, respectively15; although in normal brain it is expressed primarily in oligodendrocytes1617. The mechanism by which TPPP/p25 contributes to toxicity in Parkinson’s disease is related to its interaction with α-synuclein; their pathological complex has been considered as a potential drug target515. The physiological role of TPPP/p25 manifests itself in the differentiation of the progenitor oligodendrocytes as demonstrated by siRNA technique and specific microRNA (mir206)17. The differentiated oligodendrocytes are the major constituents of the myelin sheath.