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CNS 2016
December 05-07, 2016
Volume 7, Issue 5(Suppl) J Neurol Neurophysiol
ISSN: 2155-9562 JNN, an open access journal
conferenceseries .com
December 05-07, 2016 Dubai, UAE
2nd International Conference on
Central Nervous System Disorders & Therapeutics
Sathya M et al., J Neurol Neurophysiol 2016, 7:5(Suppl)
BACE1 expression in post-natal rat brain regions: Where goes wrong?
Sathya M1, Venkatesh M S1, Gayathri K1, Moorthi P1, Jayachandran K S1, Anusuyadevi M2
1Department of Biochemistry, Bharathidasan University, Tiruchirappalli-620024, Tamilnadu, India
2Department of Bioinformatics, Bharathidasan University, Tiruchirappalli-620024, Tamilnadu, India
S cience through decades has reported that BACE1 activity towards APP promotes toxic Aβ-generation during conditions
like Alzheimer’s disease (AD). In spite of several other proteins that are involved in AD pathology it is not clear why BACE1
alone serves as target? Age and sex are considered to be the major risk factors for AD, while their influence on BACE1 expression
yet poorly investigated. In other hand, brain has parcellation of neuronal-circuits containing 180-regions and therefore the
origin of pathogenesis become mysterious; again, why hippocampus alone delineated for cognitive decline and AD is unclear.
Therefore, present study aims to understand the levels of BACE1 expression in Post-natal-developmental (PND) stages of
rat at various brain regions. Based on human-age Vs rat-age calculation, 10-groups of Wistar rats in their PND-stages viz.,
P1, P8, P24, P30, 3M, 3M-UMF, 6-M, 9M-MF, 12-M and 24-M were used to determine the sensitive period of pathogenesis
in the present study. Vulnerability at 9-different brain regions (viz., olfactory-bulb, frontal-cortex, parietal-cortex, temporal-
cortex, occipital-cortex, hippocampus, cerebellum, hypothalamus-thalamus and pons--medulla-oblongata) were analyzed for
BACE1. Immunoblotting results show an unprecedented higher expression of BACE1 even during the first post-natal week
that contradicts literature, which states that BACE1 increases in expression during aging. Interestingly, BACE1 is found to be
significantly similar in all the PND-stages and in all the regions of brain. If BACE1 is observed to be expressed throughout
the period of life, then how does the young get spared from SAD pathogenesis is astonishing. Further, to contradict, the levels
of BACE1 is expressed with higher significant in young rather than aged. Although the level of BACE1 was down regulated
during aging, the pyramidal cell rich hippocampus had a greater expression than the neocortical regions. To corroborate, it
is inconclusive to claim BACE1 as a potent-target against AD-like pathology. Further, APP during aging has to be elucidated
given that much more substrates available for BACE1 cleavage, and speculations on region specific action of BACE1 has to be
intensively investigated to consider BACE1 as potent-target against SAD pathogenesis.
Biography
Sathya M is currently working in the Department of Biochemistry at Bharathidasan University in Trichy, India. She has published several original research papers
in the reputed journals and participated in the several scientific meetings.