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Parp mutations protect from mitochondrial toxicity in Alzheimer’s disease
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Journal Article
Parp mutations protect from mitochondrial toxicity in Alzheimer’s disease
2021
Overview
Alzheimer’s disease is the most common age-related neurodegenerative 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 dinucleotide (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 overexpressing Aβ and showed 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 toxicity. Pharmacological supplementation using NAM, a form of vitamin B that acts as a precursor for NAD
+
or a genetic mutation of PARP rescues mitochondrial defects, protects neurons against degeneration and reduces behavioural impairments in a fly model of Alzheimer’s disease. Next, we looked at links between PARP polymorphisms and vitamin B intake in patients with Alzheimer’s disease. We show that polymorphisms in the human
PARP1
gene 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 availability of NAD
+
by either vitamin B supplements or the inhibition of NAD
+
-dependent enzymes such as PARPs are potential therapies for Alzheimer’s disease.
Publisher
Nature Publishing Group UK,Springer Nature B.V,Nature Publishing Group
Subject
/ 14/28
/ 64/24
/ Adenine
/ Age
/ Alzheimer Disease - drug therapy
/ Alzheimer Disease - enzymology
/ Alzheimer Disease - genetics
/ Alzheimer Disease - pathology
/ Amyloid
/ Amyloid beta-Peptides - genetics
/ Amyloid beta-Peptides - metabolism
/ Animals
/ Animals, Genetically Modified
/ Biomedical and Life Sciences
/ Drosophila melanogaster - genetics
/ Drosophila Proteins - genetics
/ Drosophila Proteins - metabolism
/ Humans
/ Mitochondria - ultrastructure
/ Mutation
/ NAD
/ Poly (ADP-Ribose) Polymerase-1 - genetics
/ Poly (ADP-Ribose) Polymerase-1 - metabolism
/ Polymorphism, Single Nucleotide
/ Ribose
/ Toxicity
