Biology subjects

Ferretti, M. T.

Publications and source records attributed to Ferretti, M. T..

3 recordsLinked to original sources

bioRxiv2025

Flickering white light stimulation at 60 Hz induces strong, widespread neural entrainment and synchrony in healthy subjects

BackgroundWhile the effects of 40 Hz externally-induced neural entrainment have been extensively described, little is known about 60 Hz entrainment in humans. Given the role of 60 Hz in cognition, neuroplasticity and neuropsychiatric disorders, this warrants further investigation. ObjectivesThis pilot study characterizes, for the first time, the neural and somatic response to 60 Hz light entrainment in healthy volunteers, over a 3 week-period. MethodsFourteen volunteers were randomized to receive either 60 Hz flickering white light or constant light as sham (30-min sessions, for 3 weeks, 5 days a week). Neural entrainment was assessed with EEG on days 1, 5 and 19. Salivary cortisol and C-reactive protein (CRP) levels, measured with ELISA, assessed the somatic response to stimulation. Side effects and well-being were monitored via questionnaires. Results60 Hz flickering light induced a strong neural entrainment across visual, parietal, temporal and frontal cortex. The signal was highly synchronous but declined significantly by day 19 compared to day 1, indicating neural habituation. Cortisol and CRP salivary levels were unchanged and the stimulation was well tolerated. ConclusionsTo the best of our knowledge this is the first study to characterize both the neural and the somatic response to flickering light over 3 weeks. The observed neural habituation suggests that neuroplasticity could be induced with repeated stimulations over 3 weeks. 60 Hz stimulation for modulating brain activity and induce neuroplasticity has implications for our basic understanding of brain physiology as well as treatment of psychiatric disorders.

neuroscience↗

bioRxiv2024

Altered T cell reactivity to β-amyloid-related antigens in early Alzheimer's disease

There is growing evidence that the adaptive immune system and neurodegenerative Alzheimers disease (AD) are intertwined in multiple ways. Recent studies have reported alterations of the adaptive immune system in early AD stages, such as preclinical AD and mild cognitive impairment (MCI) due to AD. However, the identity of specific antigenic targets and whether the respective response is beneficial or detrimental during disease progression are still open questions. Herein, we describe cross-sectional analyses of blood and cerebrospinal fluid from three different study populations covering early AD stages. We employed high-dimensional mass cytometry, single-cell RNA-sequencing, in vitro T cell secretome analysis, and antigen presentation assays to achieve a comprehensive characterization of adaptive immune cell populations. Our results show that subjects at the stage of asymptomatic, preclinical AD can mount a CD4+ T helper cell response towards {beta}- amyloid peptide and display an early enrichment of cytotoxic CD8+ effector/TEMRA cells in CSF, combined with a less immunosuppressive gene signature of peripheral regulatory T cells. Conversely, in MCI due to AD, we observed increased frequencies of CD8+ effector/TEMRA cells in the periphery, characterized by a pro-inflammatory gene expression profile and an overall decrease in antigen responsiveness. Our results demonstrate the complexity of adaptive immune changes in early AD and suggest that it may be beneficial in the preclinical stage to promote specific CD4+ T cell responses, while in MCI it may be important to therapeutically target CD8+ T cell responses if these prove to be harmful.

immunology↗

bioRxiv2023

Early beta-amyloid accumulation in the brain is associated with peripheral T cell alterations

Fast and minimally invasive approaches for early, preclinical diagnosis of neurodegenerative Alzheimers disease (AD) are highly anticipated. Evidence of adaptive immune cells responding to cerebral {beta}-amyloidosis, one of the pathological hallmarks of AD, has raised the question of whether immune markers could be used as proxies for {beta}-amyloid accumulation in the brain. Here, we deploy multidimensional mass cytometry combined with unbiased machine learning techniques to immunophenotype peripheral blood mononuclear cells from study participants in cross-sectional and longitudinal cohorts. We show that increases in antigen-experienced adaptive immune cells in the blood, particularly CD45RA-reactivated T effector memory (TEMRA) cells, are associated with early accumulation of brain {beta}-amyloid and with changes in plasma AD biomarkers in still cognitively healthy subjects. Our results suggest that preclinical AD pathology is linked to systemic alterations of the adaptive immune system. These immunophenotype changes may help in the future to identify and develop novel diagnostic tools for early AD assessment and to better understand clinical outcomes.

immunology↗