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SUMMARY:*CANCELLED* LMB Seminar: Alpha-Synuclein and its aggregation in ne
 urodegenerative diseases - Prof Maria Grazia Spillantini\, Professor of Mo
 lecular Neurology\, University of Cambridge
DTSTART:20231211T110000Z
DTEND:20231211T120000Z
UID:TALK199750@talks.cam.ac.uk
CONTACT:Scientific Meetings Co-ordinator
DESCRIPTION:Most neurodegenerative diseases are characterised by the prese
 nce of abnormal intracellular protein inclusions. These inclusions were de
 scribed at the beginning of last century as the defining neuropathological
  features of diseases\, such as Alzheimer’s\, Pick’s and Parkinson’s
 . In Alzheimer’s\, Pick’s and several other diseases\, the inclusions 
 are made of the microtubule-associated protein tau. The filamentous inclus
 ions of Parkinson’s disease\, in the form of Lewy bodies and Lewy neurit
 es\, are made of the protein alpha-synuclein\; the same is true of the Lew
 y pathology of dementia with Lewy bodies and the glial cytoplasmic inclusi
 ons of multiple system atrophy. The importance of the assembly of tau and 
 alpha-synuclein is supported by the finding that mutations in their genes 
 cause disease. Studies on the distribution of Lewy pathology have suggeste
 d that in Parkinson’s disease alpha-synuclein aggregation begins in the 
 periphery and spreads to the brain\, resulting in pre-motor and motor symp
 toms. Besides the Lewy bodies In the substantia nigra and other brain area
 s\, smaller alpha-synuclein aggregates are present at synapses in the stri
 atum\, where they impair neurotransmitter release and contribute to the ea
 rly stages of neurodegeneration. We have generated transgenic mouse models
  with alpha-synuclein aggregates that reproduce the characteristic feature
 s of disease and that can be used for testing new therapeutic approaches. 
 Alpha-synuclein aggregation is a promising target for therapy.
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