Feinberg
Northwestern Medicine | Northwestern University | Faculty Profiles

News Center

  • Categories
    • Campus News
    • Disease Discoveries
    • Clinical Breakthroughs
    • Education News
    • Scientific Advances
  • Press Release
  • Media Coverage
  • Podcasts
  • Editor’s Picks
    • COVID-19
    • Cardiology
    • Cancer
    • Neurology and Neuroscience
    • Aging and Longevity
    • Artificial Intelligence in Medicine
  • News Archives
  • About Us
    • Media Contact
    • Share Your News
    • News Feeds
    • Social Media
    • Contact Us
Menu
  • Categories
    • Campus News
    • Disease Discoveries
    • Clinical Breakthroughs
    • Education News
    • Scientific Advances
  • Press Release
  • Media Coverage
  • Podcasts
  • Editor’s Picks
    • COVID-19
    • Cardiology
    • Cancer
    • Neurology and Neuroscience
    • Aging and Longevity
    • Artificial Intelligence in Medicine
  • News Archives
  • About Us
    • Media Contact
    • Share Your News
    • News Feeds
    • Social Media
    • Contact Us
Home » Protein May Mark Start of Neuron Dysfunction in Parkinson’s
Disease Discoveries

Protein May Mark Start of Neuron Dysfunction in Parkinson’s

By Roger AndersonMay 14, 2014
Share
Facebook Twitter Email
First author (on left) Loukia Parisiadou, PhD, research assistant professor of Radiation Oncology, and coauthor Guoxiang Liu, a postdoctoral fellow in the lab of David Gius, MD, PhD, recently published a paper in Nature Neuroscience discussing how protein LRRK2 can alter the way in which brain cells function.

Scientists have discovered a novel regulatory role for LRRK2, one of the most common genetic factors associated with Parkinson’s disease (PD).

A team of international collaborators led by Loukia Parisiadou, PhD, research assistant professor of Radiation Oncology, revealed how mutated versions of the protein LRRK2 (encoded by the gene PARK8) alter the way in which brain cells function and ultimately die.

“We now have substantial evidence that LRRK2 controls dopamine receptor activation in the part of the brain where degeneration in PD occurs,” said Parisiadou. “We also found that inhibiting this pathway could potentially alter the function of striatal projection neurons (SPNs), which help coordinate body movement.”

The findings were recently published in Nature Neuroscience. Coauthors include members of the National Institutes on Aging (NIA). Collaborators include David Gius, MD, PhD, professor of Radiation Oncology.

The scientists demonstrated that LRRK2 directs a specific kinase (PKA) in the neurons. When the protein is mutated, it begins a cascade of events that can cause the death of nerve cells. By inhibiting these mutated proteins, cell death could be prevented.

“Before we are in a position to use this knowledge to develop treatments, we need to better understand the functional role of LRRK2, particularly in neurons,” Parisiadou said. “Our findings provide a basis for further exploration of the mechanism underlying the LRRK2-mediated development of Parkinson’s disease.”

In light of LRRK2’s impact on PKA signaling, Parisiadou will attempt to uncover the potential role that LRRK2 plays in SPNs in response to dopamine depletion. The belief is that LRRK2 mutations might underlie a type of dopamine dysfunction in PD.

“It will be a great challenge to develop PKA inhibitors that selectively target the striatal neurons. Although a long way off, these findings offer a promising route for development of novel therapies and new treatments for Parkinson’s disease,” Parisiadou said.

The study was supported by the intramural research programs of the NIA and the National Institute of Alcohol Abuse and Alcoholism.

Neurology and Neuroscience Research
Share. Facebook Twitter Email

Related Posts

Transforming the Way Cancer Vaccines are Designed and Made

Jan 30, 2023

Calcium Channels Regulate Neuroinflammation and Neuropathic Pain 

Jan 27, 2023

Shortage of Mental Health Professionals Linked to Increase in Youth Suicides

Jan 25, 2023

Comments are closed.

Latest News

Medical School Faculty Named AAAS Fellows

Jan 31, 2023

Transforming the Way Cancer Vaccines are Designed and Made

Jan 30, 2023

Calcium Channels Regulate Neuroinflammation and Neuropathic Pain 

Jan 27, 2023

Changes in Medical School Leadership

Jan 26, 2023

Shortage of Mental Health Professionals Linked to Increase in Youth Suicides

Jan 25, 2023
  • News Center Home
  • Categories
  • Press Release
  • Media Coverage
  • Editor’s Picks
  • News Archives
  • About Us
Flickr Photos
Feinberg_In_Vivo_20221209_tcrawford-24
Feinberg_In_Vivo_20221209_tcrawford-16
Feinberg_In_Vivo_20221209_tcrawford-14
Feinberg_In_Vivo_20221209_tcrawford-5
Feinberg_In_Vivo_20221209_tcrawford-6
Feinberg_In_Vivo_20221209_tcrawford-10
Feinberg_In_Vivo_20221209_tcrawford-8
Feinberg_In_Vivo_20221209_tcrawford-18
Feinberg_In_Vivo_20221209_tcrawford
Feinberg_In_Vivo_20221209_tcrawford-23
Feinberg_In_Vivo_20221209_tcrawford-25
Feinberg_In_Vivo_20221209_tcrawford-26

Northwestern University logo

Northwestern University Feinberg School of Medicine

RSS Facebook Twitter LinkedIn Flickr YouTube Instagram
Copyright © 2023 Northwestern University
  • Contact Northwestern University
  • Disclaimer
  • Campus Emergency Information
  • Policy Statements

Type above and press Enter to search. Press Esc to cancel.