title: Role of apolipoprotein E polymorphism as a prognostic marker in traumatic brain injury and neurodegenerative disease: a critical review.
abstract: OBJECT The difference in course and outcome of several neurodegenerative conditions and traumatic injuries of the nervous system points toward a possible role of genetic and environmental factors as prognostic markers. Apolipoprotein E (Apo-E), a key player in lipid metabolism, is recognized as one of the most powerful genetic risk factors for dementia and other neurodegenerative diseases. In this article, the current understanding of APOE polymorphism in various neurological disorders is discussed. METHODS The English literature was searched for various studies describing the role of APOE polymorphism as a prognostic marker in neurodegenerative diseases and traumatic brain injury. The wide ethnic distribution of APOE polymorphism was discussed, and the recent meta-analyses of role of APOE polymorphism in multiple diseases were analyzed and summarized in tabular form. RESULTS Results from the review of literature revealed that the distribution of APOE is varied in different ethnic populations. APOE polymorphism plays a significant role in pathogenesis of neurodegeneration, particularly in Alzheimer's disease. APOE ε4 is considered a marker for poor prognosis in various diseases, but APOE ε2 rather than APOE ε4 has been associated with cerebral amyloid angiopathy-related bleeding and sporadic Parkinson's disease. The role of APOE polymorphism in various neurological diseases has not been conclusively elucidated. CONCLUSIONS Apo-E is a biomarker for various neurological and systemic diseases. Therefore, while analyzing the role of APOE polymorphism in neurological diseases, the interpretation should be done after adjusting all the confounding factors. A continuous quest to look for associations with various neurological diseases and wide knowledge of available literature are required to improve the understanding of the role of APOE polymorphism in these conditions and identify potential therapeutic targets.
authors.affiliation: Department of Neurosurgery, LSU Health Shreveport, Louisiana.
authors.forename: Tanmoy Kumar
authors.initials: TK
authors.lastname: Maiti
authors.affiliation: Department of Neurosurgery, LSU Health Shreveport, Louisiana.
authors.forename: Subhas
authors.initials: S
authors.lastname: Konar
authors.affiliation: Department of Neurosurgery, LSU Health Shreveport, Louisiana.
authors.forename: Shyamal
authors.initials: S
authors.lastname: Bir
authors.affiliation: Department of Neurosurgery, LSU Health Shreveport, Louisiana.
authors.forename: Piyush
authors.initials: P
authors.lastname: Kalakoti
authors.affiliation: Department of Neurosurgery, LSU Health Shreveport, Louisiana.
authors.forename: Papireddy
authors.initials: P
authors.lastname: Bollam
authors.affiliation: Department of Neurosurgery, LSU Health Shreveport, Louisiana.
authors.forename: Anil
authors.initials: A
authors.lastname: Nanda
mesh_terms: D000818:Animals; D001057:Apolipoproteins E / Q000235:genetics*; D001930:Brain Injuries / Q000175:diagnosis / Q000235:genetics*; D005819:Genetic Markers / Q000235:genetics*; D006801:Humans; D019636:Neurodegenerative Diseases / Q000175:diagnosis / Q000235:genetics*; D011110:Polymorphism, Genetic / Q000235:genetics*; D011379:Prognosis
chemical_list: D001057:Apolipoproteins E; D005819:Genetic Markers
keywords: AD = Alzheimer’s disease; ALS = amyotrophic lateral sclerosis; APOE = apolipoprotein E; Alzheimer’s disease; Aβ = amyloid β protein; CAA = cerebral amyloid angiopathy; GOS = Glasgow Outcome Scale; ICH = intracerebral hemorrhage; PD = Parkinson’s disease; SAH = subarachnoid hemorrhage; TBI = traumatic brain injury; apolipoprotein E; neurodegenerative disease; traumatic brain injury