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• W2765667078 abstract "Alzheimer's disease (AD) is the most common form of dementia. No sufficient treatment has been developed. The amyloid cascade is a leading hypothesis for AD aetiology, however drug treatments targeted at this pathology have failed to provide effective treatment. Amyloid pathology is preceded by mitochondrial dysfunction, including; abnormal mitochondrial morphology, and reduced mitochondrial membrane potential (MMP). Mitochondrial abnormalities are well characterised in Parkinson's disease (PD). Our recent work found ursodeoxycholic acid treatment (UDCA) rescues fibroblast mitochondrial abnormalities in PD patients (due to parkin and LRRK2 mutations). We hypothesised mitochondrial impairment can be identified in AD patient fibroblasts and could be rescued by UDCA treatment. 1. Investigate mitochondrial morphology and function in fibroblasts from sporadic AD (sAD), Presenilin 1 mutation (PSEN1) and controls. 2. Determine if mitochondrial function and morphology are improved in AD patient fibroblasts after treatment with UDCA. 3. Investigate if lactate production is impaired in fibroblasts from AD patients and controls. Fibroblasts were acquired from the Coriell Cell repository (3 sAD, 3 PSEN1 mutants and 3 control lines). Cellular ATP measurements were undertaken using luminescent protocols. Mitochondrial membrane potential, mitochondrial morphology, number, and cellular location were measured using tetramethylrhodamine dye and live cell imaging on the InCell 2000 high content imager. Lactate levels were measured using a lactate kit and absorbance protocol. AD fibroblasts show mitochondrial abnormalities; including reduced ATP levels (sAD 63%, p<0.05 PSEN1 24% p=0.54), reduced MMP (sAD 24% p<0.05, PSEN1 30% p<0.05) reduced mitochondrial number (25% sAD p< 0.05 and PSEN1 p<0.05) and increased perinuclear region mitochondria (sAD 4.8% p=0.08, PSEN1 8.9% p<0.05). UDCA treatment normalized ATP levels in sAD and PSEN1 fibroblasts (treated sAD vs untreated sAD p<0.0085) (treated PSEN1 vs untreated PSEN1 P=0.119). MMP and morphological abnormalities were not affected by UDCA treatment. Extracellular lactate levels in culture medium from sAD and PSEN1 fibroblasts was reduced when compared to control fibroblasts (sAD 31% p<0.05, PSEN1 52% p<0.005). These findings suggest UDCA can improve mitochondrial functional abnormalities in patient cells from multiple neurodegenerative diseases. These findings also show that lactate production is abnormal in AD fibroblasts, suggesting metabolic compromise." @default.
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• W2765667078 date "2017-07-01" @default.
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• W2765667078 title "[P4-034]: MITOCHONDRIAL ABNORMALITIES ARE FOUND IN FIBROBLASTS FROM SPORADIC ALZHEIMER's DISEASE PATIENTS: RECOVERY WITH URSODOXYCHOLIC ACID TREATMENT" @default.
• W2765667078 doi "https://doi.org/10.1016/j.jalz.2017.06.1898" @default.
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