Review Class - March 31, 2014 - LIFESCI 3B03.docx
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Department
Life Sciences
Course
LIFESCI 3B03
Professor
Margaret Fahnestock
Semester
Winter

Description
LECTURE  LIFESCI 3B03 Review Class  March 31, 2014 AD Lecture ­ Analyzing spinal fluid  o Plaques form in the brain, when they get dense, amyloid decreases in CSF – it’s all sequestered into the brain  o Tangles come later than plaques, so they are increasing in the CSF Myotonic Dystrophy ­ RNA Splicing  o Nuc repeat expansion occurs in the DNA – transcribed into RNA; RNA is longer than usual, larger domain for RNA binding proteins  (responsible for splicing) to bind to  ▯results in splicing defects + there are other effects because splicing defects does not explain the  disease entirely   RNA level  o Similar to Huntingtin Hap1 binding that is disturbed due to expansion – protein level Parkinson’s – slide 11  ▯different ways that aggregated proteins can spread from one cell to another  ­ 1) a­syn exits cell; A cell that has aga­syn – one cell with toxic protein; cell is suffering, begins to leak  ­ 2) a­syn can cross neighboring cell membrane by diffusion ­ 3) Endocytosed into neighboring cell; exocytosed out of cell to spread to others ­ 4) Exosome release – spread to other cells  ­ 5) Nanotube – thin connections (not axonal) between cytoplasm of neighboring neurons – postulated that aggregated proteins can travel along  nanotubes (skepticism; not a lot of literature and evidence + other ways that aggregated proteins spread) ­ 6) Trans synaptic – cells can secrete aggregated proteins at their synapses  o tau o a­syn ­ Any aggregated proteins can spread from neuron to neuron o Similarly – tau spreads from one part to many parts of the brain ­
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