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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:2026/phd-defence-j-f-m-smits@8F96275E-9F55-4B3F-A143-836282E12573
CREATED:20260603T090852
LOCATION:(1st floor) Auditorium, Main building De Boelelaan 1105 1081 HV Amsterdam
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 hope for A
lzheimer's research
Neurodegenerative diseases, such
as Alzheimer's, pose an increasing challenge to society due to the ag
ing population. In these conditions, nerve cells in the brain gradual
ly die off, leading to memory loss, cognitive decline, and ultimately
a loss of independence. Because neurons cannot renew themselves, dam
age is often irreversible. However, research by neuroscientist Jasper
Smits shows that not all brain cells are equally vulnerable: some po
ssess surprising protective mechanisms.
Smits investigated how
neurons cope with harmful accumulations of the protein tau, a hallmar
k of Alzheimer's. This protein can misfold and clump together, disrup
ting essential processes within the cell. He investigated why some ne
urons survive this stress while others die.
Granulovacu
olar degeneration vesicles (GVBs)
Smits' study shows that
a specific cellular process plays a key role in this. Under the infl
uence of tau clumping, neurons form so-called granulovacuolar degener
ation vesicles (GVBs). These are specialized structures that appear t
o be part of the cell's cleanup system. Their formation proves to dep
end on both the protein CK1δ and autophagy, the mechanism by which c
ells break down and recycle damaged components.
The difference
between neurons with and without these GVBs is striking. Cells withou
t GVBs show a sharp decline in protein production and eventually die.
Neurons that do form GVBs, on the other hand, continue to produce pr
oteins and survive longer. This is associated with increased producti
on of ribosomes, the structures responsible for protein synthesis. Th
is protective response occurs in tau and other diseases, but whether
they play the same protective role there has yet to be demonstrated.<
/p>
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.
M
ore information on the thesis
DESCRIPTION: 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 investigated how
neurons cope with harmful accumulations of the protein tau, a hallma
rk of Alzheimer's. This protein can misfold and clump together, disru
pting essential processes within the cell. He investigated why some n
eurons survive this stress while others die. Granulovacuolar
degeneration vesicles (GVBs)
Smits' study shows that a sp
ecific cellular process plays a key role in this. Under the influence
of tau clumping, neurons form so-called granulovacuolar degeneration
vesicles (GVBs). These are specialized structures that appear to be
part of the cell's cleanup system. Their formation proves to depend o
n both the protein CK1δ and autophagy, the mechanism by which cells
break down and recycle damaged components. The difference between neu
rons with and without these GVBs is striking. Cells without GVBs show
a sharp decline in protein production and eventually die. Neurons th
at do form GVBs, on the other hand, continue to produce proteins and
survive longer. This is associated with increased production of ribos
omes, the structures responsible for protein synthesis. This protecti
ve response occurs in tau and other diseases, but whether they play t
he same protective role there has yet to be demonstrated. Act
ive neurons
The results change the perception of brain ce
lls as passive victims of disease. Instead, they demonstrate that neu
rons actively attempt to limit damage and protect themselves against
protein stress. This insight has important societal implications. By
better understanding how these natural defense mechanisms work, resea
rchers can develop new treatments that not only target harmful protei
n clumps but also strengthen the resilience of brain cells. This open
s up the possibility for combined therapies that combat both the caus
e and the consequences of neurodegeneration.
In the longer ter
m, this can contribute to slowing disease processes such as Alzheimer
's, preserving cognitive functions longer, and improving the quality
of life for patients. Consequently, this research offers not only sci
entific progress but also a future perspective for a growing group of
people facing these devastating conditions. More information on the
thesis To GVB or not to GVB
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