Fluoride and aluminium disturb neuronal morphology, transport functions, cholinesterase, lysosomal and cell cycle activities.

Unlabelled: Fluoride and aluminium have been reported to cause severe alterations in the brain. However, their exact mechanisms of neurotoxic activities remain unknown.

Aim: This study was designed to investigate the role of fluoride and aluminium in neuronal transport, lysosomal, cell cycle protein and acetylcholinesterase activities.

Interplay of glia activation and oxidative stress formation in fluoride and aluminium exposure.

Background: Oxidative stress formation is pivotal in the action of environmental agents which trigger the activation of glial cells and neuroinflammation to stimulate compensatory mechanisms aimed at restoring homeostasis.

Aim: This study sets to demonstrate the interplay of fluoride (F) and aluminium (Al) in brain metabolism. Specifically, it reveals how oxidative stress impacts the activation of astrocytes (GFAP), mediates proinflammatory responses (microglia and B-cells: CD68 and CD 20 respectively) and shows the pattern of lipid peroxidation in the brain following fluoride and (or) aluminium treatment in vivo.

NMDA-R inhibition affects cellular process formation in Tilapia melanocytes; a model for pigmented adrenergic neurons in process formation and retraction.

Parkinson's disease has long been described to be a product of dopamine and (or) melanin loss in the substanstia nigra (SN). Although most studies have focused on dopaminergic neurons, it is important to consider the role of pigment cells in the etiology of the disease and to create an in vitro live cell model for studies involving pigmented adrenergic cells of the SN in Parkinsonism. The Melanocytes share specific features with the pigmented adrenergic neurons as both cells are pigmented, contain adrenergic receptors and have cellular processes.