Systematic Review in Neuroscience

Running head: NEUROSCIENCE
Neuroscience Systematic Review
Name of the Student
Name of the University
Author Note

1NEUROSCIENCE
Table of Contents
Abstract............................................................................................................................................2
Introduction......................................................................................................................................3
Aetiology.........................................................................................................................................4
Justification for the research question.............................................................................................5
Methods...........................................................................................................................................6
Study selection.............................................................................................................................7
Study characteristics....................................................................................................................8
Risk of bias within studies...........................................................................................................8
Results..............................................................................................................................................8
Discussion......................................................................................................................................15
Conclusion.....................................................................................................................................18
References......................................................................................................................................19

2NEUROSCIENCE
Abstract
Alzheimer's disease generally refers to a progressive neurological disease that is found to destroy
memory and other essential higher mental functions. Initially, a person suffering from
Alzheimer's disease might notice difficulty in remembering things, in addition to mild confusion.
Eventually, such individuals suffering from the disease might even forget their family members
and acquaintances, thereby undergoing dramatic personality changes. Therefore, Alzheimer's
disease is recognized as the common factor that contributes to dementia that refers to a group of
neurological disorders resulting in loss of social and intellectual skills. In Alzheimer's disease,
the neuronal cells die and degenerate, thereby causing a decline in memory. Current medications
and prevention strategies in AD often encompass administration of drugs such as donepezil, and
bapineuzumab antibody therapy for slowing down the cognitive impairment. This report contains
a systematic review of 6 articles, 3 each for the aforementioned interventions. The guidelines of
a PRISMA chart has been used for selection of the six relevant articles, following which their
major attributes and key findings have been presented in a tabular fashion. An analysis of the
results of the systematic review illustrate on the immediate effects of donepezil, and
bapineuzumab, thereby suggesting that donepezil is more effective in curing the symptoms of
AD, compared to bapineuzumab therapy.
Keywords: Alzheimer’s, disease, memory, cognitive, donepezil, bapineuzumab

3NEUROSCIENCE
Introduction
Alzheimer’s disease (AD) is a slowly progressive neurodegenerative brain disorder
extending with memory impairment as a symptom, it is the leading cause of dementia accounting
for approximately 70% of all cases (Fuller and Manford, 1999). According to recent
epidemiological studies, AD affects 20% of human population over 85 year olds.The
pathophysiology of AD is quite complex. Research studies conducted in recent years have
investigated the association between several comprehensive and possible theories that explain
the underlying pathogenesis of the neurological condition. This forms the foundation for
discovering novel therapeutic approaches that can prevent disintegration of the regions of the
brain.Accumulation of amyloid beta serves as a central pathogenic factor for the development of
AD; however, amyloid beta (Aβ) is a soluble peptide produced by the proteolytic cleavage of the
amyloid precursor protein (APP); which is a neuronal transmembrane protein (Johns, 2014). APP
is mainly cleaved by the proteolytic enzyme complex β-Secretase and in a second step the γ-
Secretase is cleaved into soluble, non-pathogenic fragments.This leads to the formation of a
cleavage fragment Aβ ( 1-42), a peptide, found to be of slightly longer length. This peptide
fragments are present in highly aggregated form and show resistance towards the degradation
process, brought about proteolytic enzymes (Morales et al., 2014). This in turn contributes
towards amyloid plaque extracellular aggregation, in combination with oxidative and secondary
toxic process. The toxic process lead to subsequent neuronal damage that is irreversible,
eventually resulting in degeneration of the nerve cells. This is further explained by the amyloid
cascade hypothesis that proposes the role of excess amyloid-beta peptide accumulation in the
onset of AD.