現在の合成生物学とシステム生物学
オープンアクセス

概要

Neuronal exosome-derived human tau toxicity on recipient cells

Shauna H. Yuan

Irresistible confusions Alzheimer’s infection (AD) is portrayed by
testimony of beta-amyloid as amyloid plaques and tau as neurofibrillary
tangles. While the dispersion of beta-amyloid is diffuse
and doesn’t relate well with sickness symptomatology, tau testimony
follows movement in a synaptically associated pathway.
Such movement is the premise of the Braack organizing for the
obsessive determination of AD, and relate with the seriousness
of patient manifestations. The infection movement recommends
spreading of pathology starting with one zone then onto the next
in the cerebrum. As of late distributed work propose that engendering
of poisonous protein tau can be interceded by exosomes.
Exosomes have a place with extracellular vesicles (EVs), which are
delivered by the cells through the late endosomal pathway. We
guessed that exosomes contain loads which could intercede spread
of poisonous proteins. We disconnected exosomes got from neuronally-
separated, human instigated pluripotent undifferentiated
cells that communicated the recurrent space of tau P301L and
V337M transformations (NiPSCEs) and infused them into the
wild-type mouse mind. We noticed neurotic changes including hyperphosphorylated
tau, cell misfortune and blebbing of the dendrites
in the beneficiary mouse neurons in vivo. The neurotic tau
additionally spread to other cortical and subcortical locales in the
two halves of the globe. These outcomes propose that exosomes
may direct engendering of neurodegeneration, which may have
suggestions for indicative and restorative potential.