మా గ్రూప్ ప్రతి సంవత్సరం USA, యూరప్ & ఆసియా అంతటా 3000+ గ్లోబల్ కాన్ఫరెన్స్ ఈవెంట్లను నిర్వహిస్తుంది మరియు 1000 కంటే ఎక్కువ సైంటిఫిక్ సొసైటీల మద్దతుతో 700+ ఓపెన్ యాక్సెస్ జర్నల్లను ప్రచురిస్తుంది , ఇందులో 50000 మంది ప్రముఖ వ్యక్తులు, ప్రఖ్యాత శాస్త్రవేత్తలు ఎడిటోరియల్ బోర్డ్ సభ్యులుగా ఉన్నారు.
ఎక్కువ మంది పాఠకులు మరియు అనులేఖనాలను పొందే ఓపెన్ యాక్సెస్ జర్నల్స్
700 జర్నల్స్ మరియు 15,000,000 రీడర్లు ప్రతి జర్నల్ 25,000+ రీడర్లను పొందుతున్నారు
Mishra N, Kumar P, Singh R1 and Sharma D
Objective: In the present study, we assessed the change in α-synuclein expression upon stereotaxic administration of pre-aggregated amyloid (Aβ40 and Aβ42) in the hippocampus and amygdala of the rat brain.
Method: Forty-eight, male Wistar rats, 6 months of age at the beginning of the experiment, were divided into 8 groups, containing 6 animals in each group. Group 1: saline injected into the hippocampus (Aβ40 Hippocampus Control). Group 2: aggregated-Aβ40injected into the hippocampus (Aβ40 Hippocampus Test). Group 3: saline injected into the amygdala (Aβ40 Amygdala Control). Group 4: aggregated-Aβ40 injected into the amygdala (Aβ40 Amygdala Test). Group 5: 16.7%DMSO in distilled water injected into the hippocampus (Aβ42 Hippocampus Control). Group 6: aggregated-Aβ42 oligomer was injected into the hippocampus (Aβ42 Hippocampus Test). Group 7: 16.7%DMSO in distilled water injected into the amygdala (Aβ42 Amygdala Control). Group 8: aggregated-Aβ42 administered into the amygdala (Aβ42Amygdala Test). Animals of each group were sacrificed by cervical dislocation (n=6) and transcardial perfusion (n=4) for molecular experiments (real-time PCR and western blotting) and histological studies, respectively. Brains were micro-dissected into amygdala, hippocampus, cortex, cerebellum, medulla, and midbrain for the molecular experiments.
Results: We found that there was an increase in the expression of α-synuclein, both at the gene and protein levels, in the hippocampus and cortex of the amyloid injected animals. Aβ42 seemed to produce a quantitatively greater effect than Aβ40.
Conclusion: Therefore, it can be extrapolated that increased expression of amyloid precursor protein (APP) gene can lead to the increase in expression of α-synuclein, leading to greater neurotoxicity in neurodegenerative disorders caused by APP overexpression (such as AD).