Pierre Hakizimana

Principal Research Engineer, Docent

About me

Pierre Hakizimana.
Photo credit: Thor Balkhed
I obtained my MSc (2004) and PhD (2008) degrees in biochemistry from the Université Libre de Bruxelles, Belgium. As a PhD student, I was investigated how protein-lipid interactions regulate antibiotic resistance in bacteria.

During mypostdoctoral studies at Karolinska Institute (Sweden), I was investigated the mechanical behavior of the sound transduction apparatus in conditions that characterise noise-induced hearing loss.

My current research at Linköping University (Sweden) is focused on molecular processes that take place during the development of noise-induced hearing loss and how these processes can be blocked to prevent hearing loss.

CV

CV

  • 2004 - MSc in biochemistry, Université Libre de Bruxelles, Belgium
  • 2008 - PhD in biochemistry, Université Libre de Bruxelles, Belgium
  • 2008-2012 - Wenner-Gren Foundations and Karolinska  Institute’s postdoctoral fellowships, Karolinska Institute, Sweden
  • 2012-2013 -  Researcher, Karolinska Institute, Sweden
  • Since 2013 -  Researcher, Linköping University
  • Chair of the Preparatory Committee, Regional Animal Experimentation Ethics Committee in Linköping

Teaching programme

  • PBL Tutor in the Introductory Course in Medical Biology
  • Course Coordinator for the Master's Course in Neurobiology since 2016

Membership, Awards and Prices

  • Membership in the Association for Research in Otolaryngology (ARO), USA
  • Tysta skolan Foundations grant
  • Torsten Söderberg Foundation grant

Publications

Cover of publication ''
Dan Bagger-Sjoback, Karin Stromback, Malou Hultcrantz, Georgios Papatziamos, Henrik Smeds, Niklas Danckwardt-Lilliestrom, Bo Tideholm, Ann Johansson, Sten Hellstrom, Pierre Hakizimana, Anders Fridberger (2015)

Scientific Reports , Vol.5 Continue to DOI

Cover of publication ''
Pierre Hakizimana, William E Brownell, Stefan Jacob, Anders Fridberger (2012)

Nature Communications , Vol.3 Continue to DOI

Cover of publication ''
Pierre Hakizimana, William E Brownell, Stefan Jacob, Anders Fridberger (2012)

Nature Communications , Vol.3 Continue to DOI

More publications

2024

Pierre Hakizimana (2024) The sensitivity of mechanoelectrical transduction response phase to acoustic overstimulation is calcium-dependent Pflügers Archiv: European Journal of Physiology, Vol. 476, p. 271-282 (Article in journal) Continue to DOI

Organisation

News

Research

Pharmacological Prevention of Hearing Damage

Over 400 million people globally suffer from hearing impairments, resulting in costs of nearly 980 billion US dollars annually. These impairments not only degrade the hearing ability of the affected individuals but also reduce their quality of life and can lead to serious issues such as depression, dementia, and learning difficulties. A study in The Lancet has shown that hearing loss is a risk factor for 8% of dementia cases, indicating that effective prevention of hearing damage could potentially reduce the number of dementia cases and associated societal costs.

Particularly vulnerable are the over one billion young adults and teenagers who regularly expose themselves to harmful noise levels when using various portable devices to listen to music or other audio. This exposure often leads to temporary threshold shift (TTS), a less severe and temporary form of hearing impairment. However, repeated episodes of TTS can eventually lead to permanent threshold shift (PTS). Soldiers in noisy combat and training environments are also at risk of hearing damage.

Despite the availability of effective modern hearing protection, such as earplugs, they are often insufficient for these groups. Young individuals frequently use in-ear headphones to listen to music. Soldiers need to maintain auditory situational awareness to detect sounds, understand speech, and localize sources, which means they cannot always rely on protective earplugs. One possible solution is pharmacological prevention.

Earlier research focused on methods using antioxidants to combat harmful molecules released in the inner ear during noise exposure, such as reactive oxygen species (ROS). However, this approach has proven inadequate. ROS tend to manifest at a later stage in the PTS cascade, meaning treatments targeting ROS might be too late in the PTS process. This underscores the need to target earlier stages in the process to effectively prevent the development of PTS.

Instead of solely focusing on combating already-released ROS after noise exposure, the emphasis should be on preventive measures that can be implemented before these harmful processes begin, thereby protecting hearing from irreversible damage.

This research project aims to prevent the transition from temporary TTS to PTS. Unlike PTS, which results in irreversible damage such as hair cell loss, TTS is characterized by reversible electrical and mechanical changes in the auditory organ. These changes are often difficult to detect because they can revert to normal before becoming visible under microscopic analysis.

A deeper understanding that TTS is a reversible condition, and how it differs from the more damaging PTS, opens doors for early intervention measures to prevent permanent hearing damage. We have recently demonstrated that reflected light confocal microscopy is fast enough to capture high-resolution images of the auditory organ during loud sound stimulation. In a separate study, we showed that the DC component (also known as summating potential, SP) of the auditory organ's electrical response can be used to characterize hearing damage electrically. In ongoing experiments, we are using AI technology to develop a clear picture of the short-term mechanical changes occurring in the auditory organ during loud sound stimulation based on these reflected light confocal microscopy images, while simultaneously tracking SP changes to create a clear fingerprint of TTS, both mechanically and electrically. Based on this fingerprint, we are testing whether these electrical and mechanical changes can be pharmacologically prevented, thereby hindering TTS from transforming into PTS.