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DTSTART:20190331T030000
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DTSTAMP:20260405T014548Z
UID:5c62dc1c2770b925424524@ist.ac.at
DTSTART:20190225T113000
DTEND:20190225T123000
DESCRIPTION:Speaker: Jerome Mertens\nhosted by Gaia Novarino\nAbstract: Spo
 radic Alzheimers Disease (AD) exclusively affects people at old age and re
 presents the overwhelming majority of all AD cases\, as genetically define
 d familial cases are the rare exception. Still\, most research on AD has b
 een performed on genetic causes and their directly related pathways\, also
  because we were in lack of models that can reflect complex human genetics
 \, physiology\, and age in an appropriate human neuronal context. While pa
 tient-specific iPSC-based models represent an attractive solution\, iPSC r
 eprogramming results in cellular rejuvenation and thus yields phenotypical
 ly young neurons. By contrast\, direct conversion of old patient fibroblas
 ts into induced neurons (iNs) preserves endogenous signatures of aging. To
  control for the involvement of aging in human neuronal models for AD\, we
  took advantage of combining both technologies and generated age-equivalen
 t fibroblast-derived iNs\, as well as rejuvenated iPSC-derived neurons fro
 m a large cohort of AD patients and controls. In addition to their rejuven
 ated state\, we found that iPSC neurons transcriptionally resemble prenata
 l developmental stages\, while iNs reflect adult-like neuronal stages and 
 show little correlation with the prenatal brain. Thus not surprisingly\, o
 nly age-equivalent adult-like iNs\, but not rejuvenated prenatal-like iPSC
  neurons\, revealed a strong AD patient-specific transcriptome signature\,
  which shows high concordance with previous human post-mortem AD studies\,
  and highlights functional gene categories known to be involved in neurode
 generation. Based on AD patient-specific transcriptional\, functional\, an
 d epigenetic changes\, we found that AD iNs display a more de-differentiat
 ed neuronal state than control iNs\, which might underlie many of the here
  and previously observed changes in AD. These data show that iNs represent
  a unique tool for studying age-related neurodegeneration\, and support a 
 view where a partially de-differentiated state of aged cells might permit 
 the loss of the specialized neuronal fitness in AD.
LOCATION:Seminar Room\, Lab Building East\, ISTA
ORGANIZER:lmarr@ist.ac.at
SUMMARY:Jerome Mertens: Next-generation human cell reprogramming to study a
 ge-related neurodegeneration
URL:https://talks-calendar.ista.ac.at/events/1808
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