Teresa Joy

N-Acetyl Cysteine Supplement Minimize Tau Expression and Neuronal Loss in Animal Model of Alzheimer’s Disease

Alzheimer’s disease (AD) is characterized by the accumulation of neurofibrillary tangles (NFT), deposition of beta amyloid plaques, and consequent neuronal loss in the brain tissue. Oxidative stress to the neurons is often attributed to AD, but its link to NFT and β-amyloid protein (BAP) still remains unclear. In an animal model of AD, we boosted the oxidative defense by N-Acetyl cysteine (NAC), a precursor of glutathione, a powerful antioxidant and free radical scavenger, to understand the link between oxidative stress and NFT. In mimicking AD, intracerebroventricular (ICV) colchicine, a microtubule disrupting agent also known to cause oxidative stress was administered to the rats. The animal groups consisted of an age-matched control, sham operated, AD, and NAC treated in AD models of rats. Cognitive function was evaluated in a passive avoidance test; neuronal degeneration was quantified using Nissl staining. NFT in the form of abnormal tau expression in different regions of the brain were evaluated through immunohistochemistry using rabbit anti-tau antibody. ICV has resulted in significant cognitive and neuronal loss in medial prefrontal cortex (MFC) and all the regions of the hippocampus. It has also resulted in increased accumulation of intraneuronal tau in the hippocampus and MFC. NAC treatment in AD model rats has reversed the cognitive loss and neuronal degeneration. The intraneuronal tau expression also minimized with NAC treatment in AD model rats. Thus, our findings suggest that an antioxidant supplement during the progression of AD is likely to prevent neuronal degeneration by minimizing the neurofibrillary degeneration in the form of tau accumulation.

Effect of Prenatal Isotretinoin on Postnatal Development of Cornea and Lens in Albino Wistar Rat: A Morphometric and Histopathlogical Analysis

Isotretinoin is a known teratogen affecting the neuronal differentiation in developing brain. Apart from its effects on brain and other craniofacial malformations, it is also known to cause failure of detachment of the lens from the surface ectoderm. Interestingly very little is known about the teratogenic effect of isotretinoin on the development of eye. Hence in the present study we evaluated the morphometric and histopathological changes in developing cornea and lens in rats during postnatal development.The pregnant rats received16mg/kg dose of isotretinoin during gestation day 1to 7 or 12 to 18. The control group received equivalent volume of vegetable oil instead of isotretinoin. The pups were sacrificed on day 7 or 14 or 30 for histopathological and morphometric analysis using haematoxylin and eosin staining.The results of the study clearly demonstrate that prenatal isotretinoin severely affects the development and growth of the cornea in both treatment regimes. There was also a considerable damage to the morphology of the lens.This preliminary animal study clearly demonstrates the teratogenic effect of isotretinoin on developing cornea and lens.