Title:The Molecular and Functional Changes of Neural Stem Cells in Alzheimer’s
Disease: Can They be Reinvigorated to Conduct Neurogenesis
Volume: 18
Issue: 5
Author(s): Ejlal Abu-El-Rub*, Ramada R. Khasawneh, Fatimah A. Almahasneh, Basma Milad Aloud and Hana M. Zegallai
Affiliation:
- Department of Basic Medical Sciences, Faculty of Medicine, Yarmouk University, Irbid, Jordan
Keywords:
Alzheimer’s disease, neural stem cells, pathogenesis, neurogenesis, neuroinflammation, neurocognitive dysfunction.
Abstract: Alzheimer’s disease (AD) is considered one of the most complicated neurodegenerative disorders,
and it is associated with progressive memory loss and remarkable neurocognitive dysfunction that
negatively impacts the ability to perform daily living activities. AD accounts for an estimated 60-80% of
dementia cases. AD's previously known pathological basis is the deposition of amyloid β (Aβ) aggregates
and the formation of neurofibrillary tangles by tau hyperphosphorylation in the cell bodies of neurons that
are located in the hippocampus, neocortex, and certain other regions of the cerebral hemispheres and limbic
system. The lack of neurotransmitter acetylcholine and the activation of oxidative stress cascade may
also contribute to the pathogenesis of AD. These pathological events can lead to irreversible loss of neuronal
networks and the emergence of memory impairment and cognitive dysfunction that can engender an
abnormal change in the personality. AD cannot be cured, and to some extent, the prescribed medications
can only manage the symptoms associated with this disease. Several studies have reported that the regenerative
abilities of neural stem/progenitor cells (NSCs) remarkably decline in AD, which disturbs the
balancing power to control its progression. Exogenous infusion or endogenous activation of NSCs may be
the ultimate solution to restore the neuronal networks in the brain of AD patients and regenerate the damaged
areas responsible for memory and cognition. In this mini-review, we will touch upon the fate of
NSCs in AD and the utilization of neurogenesis using modified NSCs to restore cognitive functions in
AD.