ATR-IR and EPR spectroscopy for detecting the alterations in cortical synaptosomes induced by aluminium stress

Molecular mechanisms of aluminum neurotoxicity: Update on adverse effects and therapeutic strategies

“…Al-induced alteration of synapse ultrastructure are characterized by decreased postsynaptic density thickness, increased synaptic cleft width, high frequency of flat synapses, and reduced number of perforated synapse (Jing et al, 2004). Increased rigidity of synaptosomes under Al exposure due to redox-dependent modulation of membrane fluidity and membrane lipid composition (Ahmed et al, 2020a) may reduce the release of synaptic vesicles into synaptic cleft (Ahmed et al, 2020b). Al was also shown to inhibit synaptic (Na +/ K +)ATPase activity and contributing to synaptic dysfunction (Silva and Gonçalves, 2003).…”

A Tribological and Ion Released Research of Ti-Materials for Medical Devices

“…Concerning the harmful effects, genotoxicity was associated with vanadium release from in vitro studies up to peripheral neuropathy and even Alzheimer’s disease [ 9 , 10 , 11 ]. Aluminum is also considered a neurotoxin, increasing the risk of degenerative diseases such as Alzheimer’s [ 12 , 13 , 14 ]. Therefore, using these materials in biomedical applications require the guarantee of no potential adverse effects of released metal cations during their exposure to biofluids.…”

Effects of aluminum chloride and coenzyme Q10 on the molecular structure of lipids and the morphology of the brain hippocampus cells

“…It represents unsaturated lipids disordering resulting from the broken double bonds in the unsaturated acyl chains during lipid peroxidation. 42 In the A group, the significant changes in the spectral features of the most intense ν as (CH 2 ) band are considered a directrix for the disordered acyl chains and increased membrane fluidity 43 that could be referred to as the formation of soluble beta-amyloid (Aβ) around the nerve cells induced by Al; 44 Aβ can alter cell functions such as lipid transport, 45 and are involved in the pathogenesis of AD. 46,47 At the same time, the significant changes in the ν s (CH 3 ) and ν s (CH 2 ) bands of the A group are indicators for the loss of acyl chain structure that happens during the trans -to- gauche transition.…”