中国神经再生研究(英文版) ›› 2020, Vol. 15 ›› Issue (12): 2195-2202.doi: 10.4103/1673-5374.284980

• 综述:退行性病与再生 • 上一篇    下一篇

FKBP12暗示神经退行性病变越来越多的证据

  

  • 出版日期:2020-12-15 发布日期:2020-08-04

Mounting evidence of FKBP12 implication in neurodegeneration

Gabriella Caminati1, 2, Piero Procacci1   

  1. 1 Department of Chemistry “Ugo Schiff ”, University of Florence, Sesto Fiorentino, Italy
    2 Center for Colloid and Surface Science (CSGI), University of Florence, Sesto Fiorentino, Italy
  • Online:2020-12-15 Published:2020-08-04
  • Contact: Gabriella Caminati,gabriella.caminati@unifi.it; Piero Procacci,piero.procacci @unifi.it.

摘要: orcid: 0000-0002-5947-7757 (Gabriella Caminati)
         0000-0003-2667-3847(Piero Procacci)

Abstract: Intrinsically disordered proteins, such as tau or α-synuclein, have long been associated with a dysfunctional role in neurodegenerative diseases. In Alzheimer’s and Parkinson’s’ diseases, these proteins, sharing a common chemical-physical pattern with alternating hydrophobic and hydrophilic domains rich in prolines, abnormally aggregate in tangles in the brain leading to progressive loss of neurons. In this review, we present an overview linking the studies on the implication of the peptidyl-prolyl isomerase domain of immunophilins, and notably FKBP12, to a variety of neurodegenerative diseases, focusing on the molecular origin of such a role. The involvement of FKBP12 dysregulation in the aberrant aggregation of disordered proteins pinpoints this protein as a possible therapeutic target and, at the same time, as a predictive biomarker for early diagnosis in neurodegeneration, calling for the development of reliable, fast and cost-effective detection methods in body fluids for community-based screening campaigns.

Key words: Alzheimer’s disease, biomarker, detections, FKBP12, FK506 binding protein, neurodegeneration, Parkinson’s disease, tau protein, α-synuclein