Review Volume 11, Issue 2 pp 787—816
Impact of Apolipoprotein E gene polymorphism during normal and pathological conditions of the brain across the lifespan
- 1 Neuropathology Research, Biomedical Research Institute of New Jersey (BRInj), Cedar Knolls, NJ 07927, USA
- 2 MidAtlantic Neonatology Associates (MANA), Morristown, NJ 07960, USA
- 3 Atlantic Neuroscience Institute, Atlantic Health System (AHS), Overlook Medical Center, Summit, NJ 07901, USA
received: June 15, 2018 ; accepted: January 5, 2019 ; published: January 24, 2019 ;https://doi.org/10.18632/aging.101757
How to Cite
Copyright: Iacono and Feltis. This is an open‐access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
The central nervous system (CNS) is the cellular substrate for the integration of complex, dynamic, constant, and simultaneous interactions among endogenous and exogenous stimuli across the entire human lifespan. Numerous studies on aging-related brain diseases show that some genes identified as risk factors for some of the most common neurodegenerative diseases - such as the allele 4 of APOE gene (APOE4) for Alzheimer’s disease (AD) - have a much earlier neuro-anatomical and neuro-physiological impact. The impact of APOE polymorphism appears in fact to start as early as youth and early-adult life. Intriguingly, though, those same genes associated with aging-related brain diseases seem to influence different aspects of the brain functioning much earlier actually, that is, even from the neonatal periods and earlier. The APOE4, an allele classically associated with later-life neurodegenerative disorders as AD, seems in fact to exert a series of very early effects on phenomena of neuroplasticity and synaptogenesis that begin from the earliest periods of life such as the fetal ones.
We reviewed some of the findings supporting the hypothesis that APOE polymorphism is an early modifier of various neurobiological aspects across the entire human lifespan - from the in-utero to the centenarian life - during both normal and pathological conditions of the brain.