Transit phases of β-amyloid and tau proteins formation and re-solubilisation in AD rat hippocampus tissue as probed by ATR-IR spectroscopy

Glucagon‐like peptide‐1 analog improves neuronal and behavioral impairment and promotes neuroprotection in a rat model of aluminum‐induced dementia

“…There was a moderately significant increase in the level of MDA (which indicates lipid peroxidation) and a moderate significant decrease in the level of SOD (which is an essential natural antioxidant) when both were compared to the control group. This goes with the previous studies which found that ALCL 3 exposure is associated with impairment of mitochondrial functions and antioxidant defense system, in vivo and in vitro (Balgoon et al., 2019). AD stimulates macroautophagy of A β that may further induce cell death by destabilizing lysosomal membranes (Al‐Okbi et al., 2017).…”

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

“…These signs were perceived in the hippocampus' neuron with loss of some cell; 56 it was proven that the AlCl 3 administration could cause the outcrop of neurotic plaques in the hippocampal tissues with a black center. 15 These observations are typical for AD disease; besides, they were observed in the rats' hippocampus brain tissues receiving only AlCl 3 . These indicators are considered clear evidence of oxidative damage and chronic inflammation.…”

“…13 Its compound, i.e., aluminum chloride (AlCl 3 ), is considered a neurotoxin due to its ability to change both lipids and proteins. 14,15 It can disturb and interfere with the acetylcholine metabolism and act as an etiopathogenic cofactor leading to neurodegenerative diseases. 16 Many studies reported the ability of AlCl 3 to alter the membrane phospholipids' structure, function, and ion homeostasis.…”

“…16 Many studies reported the ability of AlCl 3 to alter the membrane phospholipids' structure, function, and ion homeostasis. 15,17 A daily dose of one g of AlCl 3 for ten days changed the molar ratio of cholesterol/phospholipid and induced membrane uidity of cortex synaptosomes in the rat brain. 18 Therefore, antioxidants that can minimize oxidative stress or stimulate the cellular antioxidants could protect against aluminum poisoning.…”

A Potentially Detrimental Pin1 in Cerebrovascular Pathology: Beyond its Traditionally Beneficial Regulation of Amyloid–β and Tau

“…Some novel neurological studies highlight the pathogenic associations of amyloid-β, tau and genetic polymorphisms with cognitive impairment, Alzheimer's disease (AD), etc. [1][2][3][4]. To our knowledge, the pathogenic mechanisms of cognitive impairment and AD are very complicated.…”