Amelioration of social isolation-triggered onset of early Alzheimer's disease-related cognitive deficit by N-acetylcysteine in a transgenic mouse model

The Role of Mental and Physical Activities against Development of Alzheimer ’s Disease in Socialized and Isolated Rats

“…Also, AD socialized and isolated groups with mental and physical activities as compared to their corresponding AD socialized and isolated groups respectively. It is well recognized that regular exercise has favourable influence on brain function, including better memory and increased capillarization [118], brain plasticity [85] and up-regulation of the antioxidant system [119], and thus preventing the neuronal degenerative effects of SI and AD which subsequently, increase ROS and lipid peroxidation of neuronal cell membrane [14,16]. These findings are in agreement with other results of [119].…”

“…However, precise mechanism by which SI causes increase in Aβ is still not clear. Indeed, the beginning of cognition decline associated AD development is correlated well with Aβ and stress levels [14,23]. Furthermore, stress induced by SI is associated with the hippocampus as well as the frontal cortex related neuron circuits.…”

“…Social isolation (SI) as a major source of psychosocial stresses is associated with high prevalence of neurological diseases. Moreover, chronic stress that induced by SI is considered as a risk factor for development of AD [14]. Indeed, in both health and disease conditions cognition is highly susceptible to the influence of different social stressors.…”

An increased need for dietary cysteine in support of glutathione synthesis may underlie the increased risk for mortality associated with low protein intake in the elderly

“…It is reasonable to suspect that an age-related decline in brain glutathione and Nrf2 could exacerbate their progression. Indeed, NAC has shown efficacy in rodent models of these disorders (Offen et al 1996;Martinez 2000;Chen et al 2007;Clark et al 2010;Berman et al 2011;Martinez-Banaclocha 2012;Smeyne and Smeyne 2013;Moreira et al 2007;Huang et al 2010;Pocernich and Butterfield 2012;Hsiao et al 2012;Farr et al 2003). NAC is also beneficial in a mouse model of ALS (Andreassen et al 2000).…”

Molecular Alterations in the Hippocampus after Experimental Subarachnoid Hemorrhage

“…26 In the current study, the decreased expression of CamK-II (and a trend towards decreased expression of GluR1) in CA1 area of the hippocampus could explain the loss of LTP after SAH. 6 Impaired cognitive function and loss of LTP associated with decreased expression or dysfunction of GluR1 and CamK-II were found in other diseases such as Fragile X syndrome and Alzheimer disease 27,28 and in GluR1 and CamK-II knockout mice 29,30 but not GluR2 or 3 knockout mice. 31 Interestingly, IL-1b, a proinflammatory cytokine was found to impair both memory and AMPA receptor expression.…”