Study on Social Isolation as a Risk Factor in Development of AlzheimerÃ¢ÂÂs Disease in RatsAzza A Ali1*, Mona G Khalil2, Hemat A Elariny1 and karema Abu-Elfotuh1
- *Corresponding Author:
- Azza A Ali
Head of Pharmacology and Toxicology Department
Faculty of Pharmacy, Al-Azhar University, Cairo
253, Tagamoa 3, Local 7, New Cairo-11835 Egypt
Tel: +2 01061905439
E-mail: [email protected]
Received Date: April 28, 2017 Accepted Date: May 12, 2017 Published Date: May 20, 2017
Citation: Ali AA, Khalil MG, Elariny HA, Abu-Elfotuh K (2017) Study on Social Isolation as a Risk Factor in Development of Alzheimer’s Disease in Rats. Brain Disord Ther 6: 230. doi: 10.4172/2168-975X.1000230
Copyright: © 2017 Ali AA, et al.. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: Alzheimer’s disease (AD) is a neurodegenerative disease that leads to memory loss. It is characterized by deposition of Beta-amyloid peptides (Aβ), accumulation of neurofibrillary tangles and cell loss. Social isolation may exacerbate memory deficits. The risk of cognitive decline and the onset of AD may be lower by maintaining social connections and keeping mentally active. The relationship between frequent social activity and enhancing cognitive functions has been established.
Objective: Study the influence of complete social isolation for a long period on biochemical and histopathological changes as well as DNA fragmentation in the brain of normal rats. In addition, investigate the possible interaction between social isolation and development of AD using isolation-associated AD rat model.
Methods: Four groups of rats were used; 2 groups socialized and 2 isolated for four weeks. One of each socialized and isolated groups were served as control and the other served as AD groups and injected by ALCl3 (70 mg/kg, IP) every day during four weeks of isolation or socialization. Isolated rats were housed individually in cages covered with black plastic while socialized rats were randomly paired and housed in transparent covered cages. Biochemical changes in the brain as acetyl cholinesterase (ACHE), Aβ, brain derived neurotrophic factor (BDNF), monoamins (Dopamine, Serotonin, Norepinephrine), inflammatory mediators (TNF-α, IL-1β), oxidative parameters (MDA, SOD, TAC) and DNA fragmentation were estimated for all groups. Histopathological changes in the brain were also evaluated.
Results: Complete social isolation for a long period resulted in brain neurological damage indicated by significant increase in Aβ, ACHE, MDA, TNF-α, IL-1β as well as decreases in SOD, TAC, BDNF, and monoamines and confirmed by histopathological changes in different brain regions. Brain neurological damage was more severe in isolation-associated AD than in socialized condition. Isolation also enhanced the DNA fragmentation induced by AD.
Conclusion: Complete social isolation for a long period induces brain neuronal degenerations. It represents a risk factor especially when associated with AD; it increases DNA fragmentation and enhances the severity of AD development. Thus, socialization is advised especially with AD to avoid worsen or deterioration of the disease.