Dementia Today.net

Site updated at Wednesday, 22 June 2016

Living with Dementia

Scientists uncover how molecule protects brain cells in Parkinson’s disease model

  • - Dementia News
  • Apr 15, 2015
  • Comments
  • Viewed: 0
Tags: | neurodegenerative disease | parkinson's disease |

Scientists from the Florida campus of The Scripps Research Institute (TSRI) have found how a widely known but little-studied enzyme protects brain cells in models of Parkinson’s disease.

These findings could provide valuable insight into the development of drug candidates that could protect brain cells in Parkinson’s and other neurodegenerative diseases.

The study, published recently online ahead of print by the journal Molecular and Cellular Biology, focuses on the enzyme known as serum glucocorticoid kinase 1 (SGK1).

“The overexpression of SGK1 provides neuron protection in both cell culture and in animal models,” said Philip LoGrasso, a TSRI professor who led the study. “It decreases reactive oxygen species generation and alleviates mitochondrial dysfunction.”

Using a neurotoxin animal model of neurodegeneration, the study showed that SGK1 protects brain cells by blocking several pathways involved in neurodegeneration, deactivating other molecules known as JNK, GSK3β and MKK4.

Increasing SGK1 offers a potential therapeutic strategy because, as the study makes clear, there isn’t enough naturally occurring SGK1 to do the job.

“Even though the levels of naturally occurring SGK1 increases in the cell under stress, it was not enough to promote cell survival in our neurodegeneration model,” said Sarah Iqbal, the first author of the study and a member of the LoGrasso lab. “On the other hand, cell survival mechanisms tend to dominate when more SGK1 is added to the neurons.”

The LoGrasso lab plans to continue to explore SGK1 as a therapeutic possibility for Parkinson’s disease.

###

In addition to LoGrasso and Iqbal, other authors of the study, “Serum-Glucocorticoid-Inducible Kinase 1 Confers Protection in Cell-Based and in In Vivo Neurotoxin Models Via the C-Jun N-Terminal Kinase Signaling Pathway,” include Shannon Howard of TSRI. For more information on the study, see http://mcb.asm.org/content/early/2015/03/27/MCB.01510-14.full.pdf

The work was supported by the Department of Defense (grant W81XWH-12-1-0431), the National Institutes of Health (grants U01-NS057153 and GM103825), the Michael J Fox Foundation/23&Me, the Saul and Theresa Esman Foundation and a gift from the McCubbin Family.

###

Eric Sauter

.(JavaScript must be enabled to view this email address)
267-337-3859

Scripps Research Institute

Journal
  Molecular and Cellular Biology

Post a comment [ + Comment here + ]

There are no comments for this entry yet. [ + Comment here + ]




Comment
Your details

* Required field


Please enter the word you see in the image below:

Comments are moderated by our editors, so there may be a delay between submission and publication of your comment. Offensive or abusive comments will not be published.

What is dementia?

quality of care2 - prion disease1 - pre-dementia2 - alzheimer's markers1 - diet control1 - mycobacterium tuberculosis1 - elderly people1 - memory problems3 - dopamine6 - alzheimer's drug5 - visual hallucinations1 - csf1 - lewy body dementia2 - dopamine deficiency1 - overweight people1 - hydrocephalus1 - imbeciles1 - high cholesterol1 - coffee2 - sodium benzoate1 - dementia alliance1 - huntington's chorea1 - judgment1 - entorhinal cortex1 - parkinson's7 - low-density lipoprotein receptor-related protein 61 - high-cholesterol diet1 - huntington disease2 - alzheimers patients3 - sinequan1 -