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SUMMARY:Parp mutations protect from mitochondrial toxicity in Alzheimer’
 s disease - Yizhou Yu
DTSTART:20210609T150000Z
DTEND:20210609T160000Z
UID:TALK160948@talks.cam.ac.uk
CONTACT:Katharina Zuhlsdorff
DESCRIPTION:Alzheimer’s disease is the most common age-related neurodege
 nerative disorder. Familial forms of Alzheimer’s disease associated with
  the accumulation of a toxic form of amyloid-β (Aβ) peptides are linked 
 to mitochondrial impairment. The coenzyme nicotinamide adenine dinucleotid
 e (NAD+) is essential for both mitochondrial bioenergetics and nuclear DNA
  repair through NAD+-consuming poly (ADP-ribose) polymerases (PARPs). Here
 \, we analysed the metabolomic changes in flies over-expressing Aβ and sh
 owed a decrease of metabolites associated with nicotinate and nicotinamide
  metabolism\, which is critical for mitochondrial function in neurons. We 
 show that increasing the bioavailability of NAD+ protects against Aβ toxi
 city. Pharmacological supplementation using NAM\, a form of vitamin B that
  acts as a precursor for NAD+ or a genetic mutation of PARP rescues mitoch
 ondrial defects\, protects neurons against degeneration and reduces behavi
 oural impairments in a fly model of Alzheimer’s disease. Next\, we looke
 d at links between PARP polymorphisms and vitamin B intake in patients wit
 h Alzheimer’s disease. We show that polymorphisms in the human PARP1 gen
 e or the intake of vitamin B\, are associated with a decrease in the risk 
 and severity of Alzheimer’s disease. We suggest that enhancing the avail
 ability of NAD+ by either vitamin B supplements or the inhibition of NAD+-
 dependent enzymes\, such as PARPs are potential therapies for Alzheimer’
 s disease.
LOCATION:Zoom
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