Next Article in Journal
SnoRNA U50 Levels Are Regulated by Cell Proliferation and rRNA Transcription
Next Article in Special Issue
Delta Opioid Receptor and Its Peptide: A Receptor-Ligand Neuroprotection
Previous Article in Journal
Structure Prediction of Partial-Length Protein Sequences
Previous Article in Special Issue
Presence of proNGF-Sortilin Signaling Complex in Nigral Dopamine Neurons and Its Variation in Relation to Aging, Lactacystin and 6-OHDA Insults
Open AccessReview

Proteolytic Cleavage of Apolipoprotein E4 as the Keystone for the Heightened Risk Associated with Alzheimer’s Disease

Department of Biological Sciences, Science Building, Room 228, Boise State University, Boise, ID 83725, USA
Int. J. Mol. Sci. 2013, 14(7), 14908-14922; https://doi.org/10.3390/ijms140714908
Received: 6 June 2013 / Revised: 26 June 2013 / Accepted: 12 July 2013 / Published: 17 July 2013
(This article belongs to the Special Issue Pathology and Treatment of Central Nervous System Diseases)
Alzheimer’s disease (AD) is a progressive neurodegenerative disease characterized by microscopic lesions consisting of beta-amyloid plaques and neurofibrillary tangles (NFTs). The majority of cases are defined as sporadic and are likely caused by a combination of both genetic and environmental factors. Of the genetic risk factors identified, the 34 kDa protein, apolipoprotein (apo) E4, is of significant importance as APOE4 carriers account for 65%–80% of all AD cases. Although apoE4 plays a normal role in lipoprotein transport, how it contributes to AD pathogenesis is currently unknown. One potential mechanism by which apoE4 contributes to disease risk is its propensity to undergo proteolytic cleavage generating N- and C-terminal fragments. The purpose of this review will be to examine the mechanisms by which apoE4 contributes to AD pathogenesis focusing on the potential loss or gain of function that may occur following cleavage of the full-length protein. In this context, a discussion of whether targeting apoE4 therapeutically is a rationale approach to treating this disease will be assessed. View Full-Text
Keywords: apolipoprotein E; apoE4; Alzheimer’s disease; beta amyloid; neurofibrillary tangles; proteolysis; cleavage; neurodegeneration apolipoprotein E; apoE4; Alzheimer’s disease; beta amyloid; neurofibrillary tangles; proteolysis; cleavage; neurodegeneration
Show Figures

MDPI and ACS Style

Rohn, T.T. Proteolytic Cleavage of Apolipoprotein E4 as the Keystone for the Heightened Risk Associated with Alzheimer’s Disease. Int. J. Mol. Sci. 2013, 14, 14908-14922. https://doi.org/10.3390/ijms140714908

AMA Style

Rohn TT. Proteolytic Cleavage of Apolipoprotein E4 as the Keystone for the Heightened Risk Associated with Alzheimer’s Disease. International Journal of Molecular Sciences. 2013; 14(7):14908-14922. https://doi.org/10.3390/ijms140714908

Chicago/Turabian Style

Rohn, Troy T. 2013. "Proteolytic Cleavage of Apolipoprotein E4 as the Keystone for the Heightened Risk Associated with Alzheimer’s Disease" Int. J. Mol. Sci. 14, no. 7: 14908-14922. https://doi.org/10.3390/ijms140714908

Find Other Styles

Article Access Map by Country/Region

1
Only visits after 24 November 2015 are recorded.
Search more from Scilit
 
Search
Back to TopTop