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Trem-2 And Its Role In Alzheimer¿s

Trem-2 And Its Role In Alzheimer¿saf Dileep Kumar
Bag om Trem-2 And Its Role In Alzheimer¿s

Alzheimer's disease (AD), is a chronic neurodegenerative disease that causes senile decay of neurons It is the cause of 60¿70% of cases of dementia. The most common early symptom is difficulty in remembering recent events. Genetic factors such as rare variants of TREM2(triggering receptor expressed on myeloid cells-2) strongly increase the risk of developing AD, confirming the role of microglia in AD pathogenesis. In the last 5 years, several studies have dissected the mechanisms by which TREM2, as well as its rare variants affect amyloid and tau pathologies and their consequences in both animal models and in human studies. In this review, we summarize increases in our understanding of the involvement of TREM2 and microglia in AD development that may open new therapeutic strategies targeting the immune system to influence AD pathogenesis.

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  • Sprog:
  • Engelsk
  • ISBN:
  • 9786203926521
  • Indbinding:
  • Paperback
  • Sideantal:
  • 60
  • Udgivet:
  • 30. juni 2021
  • Størrelse:
  • 150x4x220 mm.
  • Vægt:
  • 107 g.
  • 2-3 uger.
  • 14. december 2024
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Beskrivelse af Trem-2 And Its Role In Alzheimer¿s

Alzheimer's disease (AD), is a chronic neurodegenerative disease that causes senile decay of neurons It is the cause of 60¿70% of cases of dementia. The most common early symptom is difficulty in remembering recent events. Genetic factors such as rare variants of TREM2(triggering receptor expressed on myeloid cells-2) strongly increase the risk of developing AD, confirming the role of microglia in AD pathogenesis. In the last 5 years, several studies have dissected the mechanisms by which TREM2, as well as its rare variants affect amyloid and tau pathologies and their consequences in both animal models and in human studies. In this review, we summarize increases in our understanding of the involvement of TREM2 and microglia in AD development that may open new therapeutic strategies targeting the immune system to influence AD pathogenesis.

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