The Effects of Vascular Cognitive Impairment on the Thickness of the Granular Cell Layer of the Dentate Gyrus within the Hippocampus in a Mouse Model

Akshaya Radhakrishnan, Nafisa Jadavji

Abstract


     Vascular Cognitive Impairment (VCI) is a form of dementia, most prevalent after Alzheimer’s Disease. However, VCI remains the second leading cause for dementia because it restricts blood flow to the brain and there are currently no treatments. There has been a positive correlation between VCI and hippocampal atrophy reported. Diet such as deficiencies in folic acid, is a modifiable risk factor for neurodegeneration. In the present study, a mouse model of VCI was combined with a deficiency in folic acid to assess hippocampal morphology. Animals were split into 4 experimental groups where they were placed into a control diet (CD) or folic acid deficient diet (FADD), and later these animals either had microcoils implanted around their common carotid arteries to model VCI or a sham, control surgery.  For hippocampal morphological analysis, the thickness of the granular cell layer of the dentate gyrus within the hippocampus was measured. It was hypothesized that a mouse model of VCI with microcoil treatment and reduced levels of folic acid would reduce blood flow, and increase cell death resulting in a reduced thickness of the granular cell layer within the dentate gyrus of the hippocampus. Our results show that thickness had an increasing trend in the in the FADD microcoil group. These data suggest that there may be an additional factor coming into play such as compensation by neural stem cells that needs to be further researched.


Keywords


Vascular Cognitive Impairment; Lesions; Hippocampus; Chronic Hypoperfusion; Folic Acid Deficiency

Full Text:

PDF

References


(1) 0’Brien, J. T. O., Erkinjuntti, T., Reisberg, B., Roman, G., Sawada, T., Pantoni, L., Bowler, J. V, Ballard, C., Decarli, C., Gorelick, P. B., Rockwood, K., Burns, A., Gauthier, S., Dekosky, S. T., and O’Brien, J. (2003) Vascular Cognitive Impairment. Lancet 2, 89–98.

(2) van de Pol, L., Gertz, H.-J., Scheltens, P., and Wolf, H. (2011) Hippocampal Atrophy in Subcortical Vascular Dementia. Neurodegener. Dis. 8, 465–469.

(3) Wen, B., Lampe, J. N., Roberts, A. G., Atkins, W. M., Rodrigues, A. D., and Nelson, S. D. (2007) NIH Public Access. October 454, 42–54.

(4) Squire, L. R. (1992) Memory and the Hippocampus : A Synthesis From Findings With Rats, Monkeys, and Humans. Psychol. Rev. 99, 195–231.

(5) Fenech, M. (2010) Folate, DNA damage and the aging brain. Mech. Ageing Dev. 131, 236–41.

(6) Shibata, M., Ohtani, R., Ihara, M., and Tomimoto, H. (2004) White matter lesions and glial activation in a novel mouse model of chronic cerebral hypoperfusion. Stroke. 35, 2598–603.

(7) Ming, G.-L., and Song, H. (2011) Adult neurogenesis in the mammalian brain: significant answers and significant questions. Neuron 70, 687–702.

(8) GRAMSBERGEN, A. (2007) Neural compensation after early lesions: A clinical view of animal experiments. Neurosci. Biobehav. Rev. 31, 1088–1094.




DOI: https://doi.org/10.13034/jsst.v11i1.273

Refbacks

  • There are currently no refbacks.


Copyright (c) 2019 Journal of Student Science and Technology