Topic: CD68

Background: Amyotrophic lateral sclerosis (ALS) is an intractable neurodegenerative disease of the central nervous system. Despite an unknown etiology, its pathophysiology is considered to be heterogeneous. Recent reports have highlighted the presence of disease-associated microglia (DAM) in the lesions of various neurodegenerative diseases, including that in ALS model animals. However, limited information is available regarding DAM in sporadic cases of ALS in humans.Methods: This study analyzed data from 30 patients with ALS. Autopsy samples of cervical and lumbar lesions obtained from each p

Fragile X Syndrome (FXS) is the most common neurodevelopmental disorder associated with intellectual disabilities. In FXS, an increased CGG triplet repetition in the fmr1 gene, cause the hypermethylation of the 5’UTR and, in turn leads to the gene silencing and the absence of the Fragile X mental retardation protein (FMRP). FMRP is an RNA binding protein, able to regulate the expression of different RNAs and fundamental for synapses function. FMRP is expressed in neurons but also in astrocytes and microglia, the other key cells of the brain. Despite many studies have focused their attentions o

Transcranial magnetic stimulation (TMS) is a non-invasive brain stimulation technique for modulating neocortical excitability in humans. Repetitive magnetic stimulations (rMS) applied to tissue cultures trigger functional changes of dendritic spines alongside a potentiation of excitatory neurotransmission. Furthermore, in vivo studies involving both animal models and patients have demonstrated the therapeutic potential of rTMS in treating psychiatric disorders.Despite its use in both neuroscience research and clinical settings, the molecular mechanisms of rTMS-based interventions remain not we

Alzheimer’s Disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-β (Aβ) and tau neuropathology, neuroinflammation, lipid dysregulation, and progressive loss of cognitive functioning. We have evidence that early dietary interventions with ω6/ω3 polyunsaturated fatty acids (PUFAs) can protect against cognitive decline and lastingly alter microglia and brain lipid profile in the context of early-life stress​. PUFAs can directly modulate microglia. In the context of AD, it is unknown if lipid and PUFA derivatives (oxylipins) are dysregulated in the brain, how these rel

Prostaglandins play a key role in modulating the inflammatory response in the central nervous system. They are synthesized from arachidonic acid via the enzyme cyclooxygenases (COX). The Cox-1 isoform is highly enriched in microglia. In response to infection or tissue damage, microglia become reactive which is associated with phagocytosis and pro-inflammatory function. Concurrently, selective Cox-1 inhibition has been shown to ameliorate pathological effects in several neurodegenerative diseases. So far, it is not known which impact Cox-1 expression has on the regulation of microglia activity.

Alzheimer's Disease (AD), responsible for the majority of dementia cases, is a progressive neurodegenerative disorder marked by amyloid-β accumulation, tauopathy, neuroinflammation, and cognitive decline. Parallel to this cognitive decline, the number of memory-related neurons (engram cells) is reduced in the APPswe/PSEN1dE9 mouse model for slow-progressing AD, crossed with a genetically modified mouse line that allows us to visualize engram neurons (Arc::dVenus mice). We hypothesize that aberrant microglial modulation of engram cells might contribute to the AD-related changes in engram and co

Aβ plays an important role in the pathogenesis of Alzheimer’s disease (AD), and passive immunotherapy targeting Aβ has emerged as a promising treatment approach. However, the administration of antibody drugs is limited due to many concerns. Therefore, using adeno-associated virus (AAV) gene therapy to deliver antibody drugs may introduce innovative treatment regimens for AD. We have previously shown that NP106, a novel anti-Aβ antibody, exhibits multiple therapeutic benefits for ameliorating brain Aβ burden and cognitive impairment in APP/PS1 mouse model of AD. In this study, we developed an N