Topic: glutamatergic neurotransmission

Despite extensive research, effective treatment for Alzheimer’s disease (AD) remains elusive. Emerging evidence suggests that the endocannabinoid system and glutamatergic neurotransmission play important roles in AD pathophysiology. This project aims to elucidate the involvement of cannabinoid type 1 receptor (CB1R) on regulating the cytotoxic effects induced by N-methyl-D-aspartate receptors (NMDARs) in AD. On the one hand, CB1R activation reduces neuroinflammation and promotes neuroprotection in AD models. On the other hand, the synaptic receptor NR2A contribute to synaptic integrity and mem

Environmental stress plays a key role in the development of psychiatric disorders, and also has a negative impact on sleep integrity. Insomnia and sleep disturbances are core symptoms observed in patients with stress-related disorders. However, stress reactivity is the result of a combination of genetic and environmental influences that ultimately impacts one’s physiology and behavior in a variety of ways. In this project we will focus on stress susceptibility and how it could trigger psychiatric diseases in a peculiar gene-environment interaction.Studying glutamatergic neurotransmission, we d

Repetitive transcranial magnetic stimulation (rTMS) is a widely used method of non-invasive brain stimulation in both research and clinical settings, aimed at inducing synaptic plasticity and targeting conditions like pharmaco-resistant depression and post-traumatic stress disorder. However, the detailed molecular mechanisms underlying rTMS-induced plasticity remain not well understood. N6-methyladenosine (m6A) is the most prevalent modification in the human transcriptome. m6A is known for its reversible nature and thus is a prime candidate for modulating synaptic plasticity via gene expressio

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are adult-onset neurodegenerative disorders that share common pathology and genetic causes. In many cases the RNA binding protein TDP-43 aggregates in the cytoplasm leading to the loss of its nuclear functions, including as a splicing repressor. This results in the erroneous inclusion of intronic sequences known as cryptic exons (CEs) in several mature mRNAs. Recently, it has been shown that TDP-43 depletion leads to CE inclusion in UNC13A, which encodes a protein crucial for priming synaptic vesicles for release. The UNC13A