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Biology subjects

Bolt, E.

Publications and source records attributed to Bolt, E..

3 recordsLinked to original sources

Hearing and cognitive decline in aging differentially impact neural tracking of context-supported versus random speech across linguistic timescales

Cognitive decline and hearing loss are common in older adults and often co-occur while investigated separately, affecting the neural processing of speech. This study investigated the interaction between cognitive decline, hearing loss, and contextual cues in speech processing. Participants aged 60 years and older were assessed for cognitive decline using the Montreal Cognitive Assessment and for hearing ability using a four-frequency pure tone average. They listened to in-house-designed matrix-style sentences that either provided supportive context or were random, while we recorded their electroencephalography. Neurophysiological responses were analyzed through auditory evoked potentials and speech tracking at different linguistic timescales (i.e., phrase, word, syllable and phoneme rate) using phase-locking values. The results showed that cognitive decline was associated with a lower chance of correct responses in a speech recognition task. Cognitive decline significantly impacted the P2 component of auditory evoked potentials, while hearing loss influenced speech tracking at the word and phoneme rates, but not at the phrase or syllable rates. Contextual cues enhanced speech tracking at the syllable rate. These findings suggest that cognitive decline and hearing loss differentially affect the neural mechanisms underlying speech processing, with contextual cues playing a significant role in enhancing syllable rate tracking. This study emphasises the importance of considering both cognitive and auditory factors when studying speech processing in older people and highlights the need for further research to investigate the interplay between cognitive decline, hearing loss and contextual cues in speech processing.

neuroscience↗

The monologue of the double: allocentric reduplication of the own voice alters bodily self perception

During autoscopic phenomena, people perceive a double of themselves in extrapersonal space. Such clinical allocentric self-experiences often co-occur with auditory hallucinations, yet experimental setups to induce similar illusions in healthy participants have been limited to visual doubles. We investigated whether feeling the presence of an auditory double could be provoked in healthy participants and how it might affect spatial aspects of bodily self-consciousness. We recorded the own versus another persons voice while walking around in the room using binaural headphones from an egocentric and an allocentric perspective. In comparison to listening to their own moving voice egocentrically, when listening to themselves allocentrically, participants reported a strong feeling of a presence with a similarly high degree of self-identification, suggesting a successful induction of the feeling of an acoustic doppelganger. When pointing to the source of the own voice participants localized it closer to themselves than when listening to another persons voice, suggesting a change in spatial perception. Interestingly, the opposite pattern was found in participants that had previous hallucinatory experiences. These findings show that listening to ones own voice allocentrically can manipulate bodily self-consciousness and self-related spatial perception. This paradigm enables the experimental study of the relationship between auditory vocal hallucinations and bodily self-consciousness, bridging important clinical phenomena and experimental knowledge.

neuroscience↗

Interaction of HelQ helicase with RPA modulates RPA-DNA binding and stimulates HelQ to unwind DNA through a protein roadblock.

Cells reactivate compromised DNA replication forks using enzymes that include DNA helicases for separating DNA strands and remodelling protein-DNA complexes. HelQ helicase promotes replication-coupled DNA repair in mammals in a network of interactions with other proteins. We report newly identified HelQ helicase activities, when acting alone and when interacting with RPA. HelQ helicase was strongly inhibited by a DNA-protein barrier (BamHIE111A), and by an abasic site in the translocating DNA strand. Interaction of HelQ with RPA activated DNA unwinding through the protein barrier, but not through the abasic site. Activation was lost when RPA was replaced with bacterial SSB or DNA binding-defective RPA, RPAARO1. We observed stable HelQ-RPA-DNA ternary complex formation, and present evidence that an intrinsically disordered N-terminal region of HelQ (N-HelQ) interacts with RPA, destabilising RPA-DNA binding. Additionally, SEC-MALS showed that HelQ multimers are converted into catalytically active dimers when ATP-Mg2+ is bound. HelQ and RPA are proposed to jointly promote replication fork recovery by helicase-catalysed displacement of DNA-bound proteins, after HelQ gains access to ssDNA through its N-terminal domain interaction with RPA.

biochemistry↗