Paul Kinnon (Italy)
Diadem srl
Diagnostics
Paul is the CEO of Diadem srl and has over 30 years of experience in the global life sciences industry, with the past 25 years of his executive career focused on Clinical Diagnostics and innovative products to improve patients’ lives. He has held leadership positions within PredictImmune, Transgenomic, ZyGEM Corp., Life Technologies (now ThermoFisher), Guava Technologies and Cellomics, raising more than $100m in funding, creating global partnerships and increasing shareholder return. Paul has spent half of his career living and working in the USA running global businesses, which gives him a novel and unique outlook on the global industry; additionally he sits on a number of Boards as non-executive director (NED) for Life Science companies, where he mentors and provides guidance to other CEOs. Paul has a proven strategic and commercialisation track record of identifying and bringing novel technologies and products to global market rapidly and using the most effective channels, in addition to over ten years’ international Board experience in both private and public companies, with significant expertise in Corporate governance, Corporate restructuring, M&A and divestiture activities.

Presenter of 1 Presentation

 Conference Calendar

U-P53AZ-PTMS AS FINGERPRINTS TO DETECT ALZHEIMER’S DISEASE AND OTHER DEMENTIA.

Session Name
1540 - AD, LBD DIAGNOSIS, IMAGING & CLINICAL TRIALS (ID 79)
Session Type
SYMPOSIUM
Date
Sat, 19.03.2022
Session Time
09:10 AM - 11:10 AM
Room
ONSITE: 113
Lecture Time
09:40 AM - 09:55 AM
Presenter

Abstract

Aims

Recently, the p53 protein has gained attention for its role in the early evolution of Alzheimer’s disease (AD). p53 is regulated by post translational modifications (PTMs) which affect its conformation and function in several processes in AD. We have investigated the PTMs occurring in U-p53AZ in patients suffering by different forms of dementia and at different stage of cognitive decline to show the specificity of U-p53AZ in AD.

Methods

U-p53AZ isolated from 48 patients (55 plasma samples) from AIBL biobank (70y av.) was analysed by AlzoSure®Confirm method to detect its PTMs. U-p53AZ captured by 2D3A8Ab from plasma samples fwas sequenced by mass spectrometry technology (Orbitrap XL). The study cohort included 16AD, 9 Cognitive Normal (CN), 6 Mild Cognitive Impaired (MCI), 7 asymptomatic AD, 8 prodromal AD, 6 Frontotemporal Dementia (FTD), 1 Vascular Dementia and 1 Lewy Body Dementia patients.

Results

11 U-p53AZ-PTMs of (acetylation, phosphorylation and ubiquitination in different aa-residues) were identified in total and each clinical group showed the same combination of PTMs: all AD patients showed the same PTMs pattern plus the truncation of the protein in the N-terminus region, whilst FTD showed only 3 PTMs and any truncation. Interestingly, asymptomatic and prodromal AD individuals showed a distinct PTMs pattern than CN and MCI.

Conclusions

U-p53AZ undergoes to different biochemical pathways impacting on its linear sequence specifically linked to dementia pathogenesis. U-p53AZ-PTMs detected by AlzoSure® Confirm represents a simple, non-invasive tool to discriminate AD from other dementia and to identify the stage of cognitive decline.

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