Topic: TNFα

Neuroinflammation is a fundamental element of many neurodegenerative disorders. Activation of astrocytes and microglia cells leads to a release of cytokines and reactive oxygen species followed by leakage of the blood-brain barrier and neurotoxicity. Transient neuroinflammation is understood to be largely protective, chronic neuroinflammation, however, contributes to the pathology of Alzheimer’s disease, traumatic brain injury, and many more. In this study, we focus on the aspect of cytokine-induced neuroinflammation in human microglia cells and especially in astrocytes, since many studies on

VPS10P domain receptors are intracellular sorting receptors which direct their protein cargo to destined subcellular localizations. Although it seemed that functions of VPS10P receptors in the brain are restricted to neurons, it turned out they are also relevant for glial cells, including microglia, which dependently on pathological context may acquire different functional properties. For instance, during glioblastoma progression, microglia along with infiltrating macrophages are reprogrammed, so instead of fighting with glioma they support it, mainly through secretion of pro-tumorigenic facto

A growing body of evidence emphasizes that hypometabolism taking place in astrocytes may compromise their physiological neuro-supportive role and activate a set of pathophysiological pathways contributing to the progression of neurodegenerative diseases, including Alzheimer disease (AD) [1]. Here, we explored the potential role of astrocytes in driving a cascade of detrimental effects in the neighboring neurons and investigated a possible approach to limit the injury in both cell types [2]. To this aim, primary rat cortical astrocytes were exposed to glyceraldehyde (GA) to induce a metabolic s

Patients with liver cirrhosis show hyperammonemia and peripheral inflammation and may show hepatic encephalopathy with cognitive impairment, reproduced by rats with chronic hyperammonemia. Peripheral inflammation induces neuroinflammation in hippocampus of hyperammonemic rats, altering neurotransmission and leading to cognitive impairment. Extracellular vesicles (EVs) may transmit pathological effects from the periphery to the brain. The aims were to assess whether EVs from plasma of hyperammonemic rats (HA-EVs) induce cognitive impairment and to identify the underlying mechanisms.HA-EVs were

The interaction of amyloid-beta and microtubule-associated protein tau, the two hallmark proteins of Alzheimer’s disease (AD) age-related pathology, that cause disruption of synaptic long-term potentiation and depression (LTP and LTD, respectively) is still poorly understood. Here, we recorded field excitatory postsynaptic potentials from the CA1 stratum radiatum in young and middle-aged rats under urethane anesthesia to examine the disruptive action of synaptotoxic tau in recombinant protein preparations or aqueous brain extracts from patients with AD and Pick’s disease (PiD) tauopathy. A sin