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PRODID:-//Vrije Universiteit Amsterdam//NONSGML v1.0//EN
NAME:PhD defense A.L.M.N. Toda Robert
METHOD:PUBLISH
BEGIN:VEVENT
DTSTART:20261007T134500
DTEND:20261007T151500
DTSTAMP:20261007T134500
UID:phd-defense-a-l-m-n-toda-rober@8F96275E-9F55-4B3F-A143-836282E12573
CREATED:20260924T214741
LOCATION:Main building VU, 1105, Auditorium, De Boelelaan, 1081 HV, Amsterdam
SUMMARY:PhD defense A.L.M.N. Toda Robert
X-ALT-DESC;FMTTYPE=text/html: <html> <body> <p><p>Metabolism at the cr
 ossroads of microglial function and inflammation</p></p> <p>Diseases 
 like Alzheimer's and general brain aging are major health challenges 
 driven by chronic, damaging inflammation in the brain. Microglia act 
 as the brain's primary housekeeper and defender cells, but during dis
 ease they can become persistently inflamed and dysfunctional. Until n
 ow, little was known about how human microglia store and process fats
  compared to animal models. This research focused on understanding ho
 w fat storage, fat burning, and internal cell delivery systems contro
 l how human brain immune cells trigger inflammation.</p><p>In conditi
 ons like Alzheimer's disease, microglia accumulate excess fat droplet
 s, which impairs their protective functions and triggers harmful infl
 ammatory signals. This research showed that one commonly used laborat
 ory model appeared to accumulate high levels of fat droplets, which c
 ould mask specific experimental results depending on what was being s
 tudied. By adding a key nutrient to the environment, the cells return
 ed to a healthy state of homeostasis, effectively refining an already
  valuable research tool for the field.</p><p>Additionally, the study 
 demonstrated that excess fat directly switches on inflammatory alarms
 , and that a key protein helps direct internal cell transport to cont
 rol these immune signals.</p><p>More information on the <a href="http
 s://hdl.handle.net/1871.1/daae2704-fab2-41c4-b065-5f2741c1480f">thesi
 s</a>.</p> </body> </html>
DESCRIPTION: Metabolism at the crossroads of microglial function and i
 nflammation Diseases like Alzheimer's and general brain aging are maj
 or health challenges driven by chronic, damaging inflammation in the 
 brain. Microglia act as the brain's primary housekeeper and defender 
 cells, but during disease they can become persistently inflamed and d
 ysfunctional. Until now, little was known about how human microglia s
 tore and process fats compared to animal models. This research focuse
 d on understanding how fat storage, fat burning, and internal cell de
 livery systems control how human brain immune cells trigger inflammat
 ion.In conditions like Alzheimer's disease, microglia accumulate exce
 ss fat droplets, which impairs their protective functions and trigger
 s harmful inflammatory signals. This research showed that one commonl
 y used laboratory model appeared to accumulate high levels of fat dro
 plets, which could mask specific experimental results depending on wh
 at was being studied. By adding a key nutrient to the environment, th
 e cells returned to a healthy state of homeostasis, effectively refin
 ing an already valuable research tool for the field.Additionally, the
  study demonstrated that excess fat directly switches on inflammatory
  alarms, and that a key protein helps direct internal cell transport 
 to control these immune signals.More information on the <a href="http
 s://hdl.handle.net/1871.1/daae2704-fab2-41c4-b065-5f2741c1480f">thesi
 s</a>.
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