BEGIN:VCALENDAR VERSION:2.0 PRODID:-//Vrije Universiteit Amsterdam//NONSGML v1.0//EN NAME:PhD defence J.F.M. Smits METHOD:PUBLISH BEGIN:VEVENT DTSTART:20260519T094500 DTEND:20260519T111500 DTSTAMP:20260519T094500 UID:phd-defence-j-f-m-smits@8F96275E-9F55-4B3F-A143-836282E12573 CREATED:20260922T005326 LOCATION: SUMMARY:PhD defence J.F.M. Smits X-ALT-DESC;FMTTYPE=text/html:

To GVB or not to GVB

New insights into resilient brain cells offer hop e for Alzheimer's research

Neurodegenerative diseases , such as Alzheimer's, pose an increasing challenge to society due to the aging population. In these conditions, nerve cells in the brain gradually die off, leading to memory loss, cognitive decline, and ult imately a loss of independence. Because neurons cannot renew themselv es, damage is often irreversible. However, research by neuroscientist Jasper Smits shows that not all brain cells are equally vulnerable: some possess surprising protective mechanisms.

Smits investigat ed how neurons cope with harmful accumulations of the protein tau, a hallmark of Alzheimer's. This protein can misfold and clump together, disrupting essential processes within the cell. He investigated why some neurons survive this stress while others die.

Gran ulovacuolar degeneration vesicles (GVBs)
Smits' study sho ws that a specific cellular process plays a key role in this. Under t he influence of tau clumping, neurons form so-called granulovacuolar degeneration vesicles (GVBs). These are specialized structures that a ppear to be part of the cell's cleanup system. Their formation proves to depend on both the protein CK1δ and autophagy, the mechanism by which cells break down and recycle damaged components.

The diff erence between neurons with and without these GVBs is striking. Cells without GVBs show a sharp decline in protein production and eventual ly die. Neurons that do form GVBs, on the other hand, continue to pro duce proteins and survive longer. This is associated with increased p roduction of ribosomes, the structures responsible for protein synthe sis. This protective response occurs in tau and other diseases, but w hether they play the same protective role there has yet to be demonst rated.

Active neurons
The results change th e perception of brain cells as passive victims of disease. Instead, t hey demonstrate that neurons actively attempt to limit damage and pro tect themselves against protein stress. This insight has important so cietal implications. By better understanding how these natural defens e mechanisms work, researchers can develop new treatments that not on ly target harmful protein clumps but also strengthen the resilience o f brain cells. This opens up the possibility for combined therapies t hat combat both the cause and the consequences of neurodegeneration.< br>
In the longer term, this can contribute to slowing disease pro cesses such as Alzheimer's, preserving cognitive functions longer, an d improving the quality of life for patients. Consequently, this rese arch offers not only scientific progress but also a future perspectiv e for a growing group of people facing these devastating conditions.< /p>

More information on the thesis

DESCRIPTION: To GVB or not to GVB New insights into resilient brain cells offer hope for Alzheimer's research

Neuro degenerative diseases, such as Alzheimer's, pose an increasing challe nge to society due to the aging population. In these conditions, nerv e cells in the brain gradually die off, leading to memory loss, cogni tive decline, and ultimately a loss of independence. Because neurons cannot renew themselves, damage is often irreversible. However, resea rch by neuroscientist Jasper Smits shows that not all brain cells are equally vulnerable: some possess surprising protective mechanisms.Sm its investigated how neurons cope with harmful accumulations of the p rotein tau, a hallmark of Alzheimer's. This protein can misfold and c lump together, disrupting essential processes within the cell. He inv estigated why some neurons survive this stress while others die.Granulovacuolar degeneration vesicles (GVBs)
Smits' st udy shows that a specific cellular process plays a key role in this. Under the influence of tau clumping, neurons form so-called granulova cuolar degeneration vesicles (GVBs). These are specialized structures that appear to be part of the cell's cleanup system. Their formation proves to depend on both the protein CK1δ and autophagy, the mechan ism by which cells break down and recycle damaged components.The diff erence between neurons with and without these GVBs is striking. Cells without GVBs show a sharp decline in protein production and eventual ly die. Neurons that do form GVBs, on the other hand, continue to pro duce proteins and survive longer. This is associated with increased p roduction of ribosomes, the structures responsible for protein synthe sis. This protective response occurs in tau and other diseases, but w hether they play the same protective role there has yet to be demonst rated.Active neurons
The results change the perce ption of brain cells as passive victims of disease. Instead, they dem onstrate that neurons actively attempt to limit damage and protect th emselves against protein stress. This insight has important societal implications. By better understanding how these natural defense mecha nisms work, researchers can develop new treatments that not only targ et harmful protein clumps but also strengthen the resilience of brain cells. This opens up the possibility for combined therapies that com bat both the cause and the consequences of neurodegeneration.

In the longer term, this can contribute to slowing disease processes such as Alzheimer's, preserving cognitive functions longer, and impro ving the quality of life for patients. Consequently, this research of fers not only scientific progress but also a future perspective for a growing group of people facing these devastating conditions.More inf ormation on the thesis END:VEVENT END:VCALENDAR