Reach Us +1 218 451 2974
Lessons From Cathepsin Deficient Mice On Human Brain Diseases | 31885
ISSN: 2155-9562

Journal of Neurology & Neurophysiology
Open Access

Like us on:

OMICS International organises 3000+ Global Conferenceseries Events every year across USA, Europe & Asia with support from 1000 more scientific Societies and Publishes 700+ Open Access Journals which contains over 50000 eminent personalities, reputed scientists as editorial board members.

Open Access Journals gaining more Readers and Citations
700 Journals and 15,000,000 Readers Each Journal is getting 25,000+ Readers

This Readership is 10 times more when compared to other Subscription Journals (Source: Google Analytics)
All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.

Lessons from cathepsin deficient mice on human brain diseases

4th International Conference and Exhibition on Neurology & Therapeutics

Hiroshi Nakanishi

ScientificTracks Abstracts: J Neurol Neurophysiol

DOI: 10.4172/2155-9562.S1.025


A group of proteases in the endosomal/lysosomalproteolytic system have been designated as cathepsins, which is derived
from the Greek term meaning “to digest”. Considering that cathepsins can irreversibly cleave peptide bonds, the primary
function of cathepsins has been believed to be their “disintegration actions”. However, there is increasing evidence that
cathepsins can also exert “modulator actions” by which substrates are activated after limited cleavage. For examples, we have
recently found that cathepsin B (CatB) is involved in the maturation of pro-IL-1 through proteolytic activation of pro-caspase-1
in the autophagosomes of spinal microglia following peripheral inflammation, leading to the induction and maintenance of
inflammatory pain. On the other hand, cathepsin S (CatS) is involved in proteolytic processing of the MHC class II-associated
invariant chain in splenicdendritic cells following peripheral nerve injury, leading to activation of CD4+ T cells. Infiltration of
activated CD4+ T cells may contribute to transition of nerve injury-induced acute pain to a chronic pain state. Beyond a bulk
proteolysis in the endosomal/lysosomal system, the growing understanding of modulator actions of cathepsins in microglia and
other mononuclear phagocytes could contribute to the development of protease inhibitors as therapeutic interventions against
brain diseases associated with chronic inflammation and immune response.


Hiroshi Nakanishi is currently a Professor of Department of Aging Science and Pharmacology, Kyushu University, Japan. He completed his PhD in Kyushu
University and his post-doctoral trainingin the University of Tennessee at Memphis. He became a Professor of Laboratory of Oral Aging Science, Kyushu University
in 2000. He was the Dean of Faculty of Dental Science, Kyushu University from 2011 to 2013. He is now the vice Dean Faculty of Dental Science, Kyushu University
from 2014. His research is focusing on the physiological and pathological functions of microglia in the central nervous system.

Relevant Topics