In Brains Damaged by MS or Age, Cells Can Be Tricked to Promote Remyelination, Study Suggests

In Brains Damaged by MS or Age, Cells Can Be Tricked to Promote Remyelination, Study Suggests

Publication date: Aug 20, 2019

This post was originally published on this site Our brains – much like our joints – stiffen with age, causing brain stem cells called oligodendrocyte progenitor cells (OPCs) to lose their ability to proliferate and transform into oligodendrocytes, the cells that produce myelin, an essential component for nerve cell communication, a study found. -We were fascinated to see that when we grew young, functioning rat brain stem cells on the stiff material, the cells became dysfunctional and lost their ability to regenerate, and in fact began to function like aged cells,” Kevin Chalut, one of the study’s co-lead authors, said in a press release. -When we removed Piezo1 from the surface of aged brain stem cells, we were able to trick the cells into perceiving a soft surrounding environment, even when they were growing on the stiff material,” said Robin Franklin, the study’s co-lead author. The team then mimicked the myelin damage seen in MS in the brain of aged animals, and lowered the levels of Piezo1 in OPCs. -We were able to delete Piezo1 in the OPCs within the aged rat brains, which lead to the cells becoming rejuvenated and once again able to assume their normal regenerative function,” Franklin said. -The Cambridge team’s discoveries on how brain stem cells age and how this process might be reversed have important implications for future treatment, because it gives us a new target to address issues associated with aging and MS, including how to potentially regain lost function in the brain,” Kohlhaas added.

Concepts Keywords
Aging Remyelination
Brain Stem cells
Brain Stem Oligodendrocyte progenitor cell
Cambridge Neuroscience
Central Nervous System Branches of biology
Disability Glial cells
Extracellular Matrix Neurodegenerative diseases
Lesion MS
Matrix Lesion site
Microenvironment
Multiple Sclerosis
Myelin
Nature
Nerve
Neurodegenerative Diseases
Oligodendrocytes
OPC
Progenitor Cells
Relentless
Robin
Sensor
Stiffness

Semantics

Type Source Name
drug DRUGBANK Nonoxynol-9
disease MESH development
gene UNIPROT MAGEE1
gene UNIPROT PIEZO1
pathway BSID Release
pathway BSID Aging
disease MESH aging
disease DOID multiple sclerosis
pathway BSID Neurodegenerative Diseases
disease MESH multiple sclerosis
disease MESH neurodegenerative diseases
gene UNIPROT SLC35G1
gene UNIPROT DESI1
gene UNIPROT RENBP

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