NDLI: What is the dominant aβ species in human brain tissue? A review

Content Provider	Springer Nature Link
Author	Gregory, Gillian C. Halliday, Glenda M.
Copyright Year	2005
Abstract	Epub ahead of print: December 2004 Interest in the beta amyloid (Aβ) peptides continues to grow due to their known accumulation in the brains of patients with Alzheimer’s disease and recent tantalising evidence that reducing such accumulations can reverse disease-associated functional deficits. Aβ peptides are naturally produced in every cell by proteolytic cleavage of the amyloid precursor protein with two main alloforms (40 or 42 amino acids) both of which are disease associated. The identification that genetic mutations causing Alzheimer’s disease impact on Aβ production and clearance have allowed for the manipulation of these pathways in cellular and animal models. These studies show that the amount and type of Aβ in the brain has significant consequences on neural function. However, there have been significant difficulties in the conversion of these findings into successful treatments in humans. In this review we concentrate on data from human studies to determine any comparative differences in Aβ production and clearance that may assist with better treatment design and delivery. Aβ$_{40}$ is the dominant peptide species in human cerebrospinal fluid accounting for approximately 90% of total Aβ under normal conditions. However, similar studies using disease free human brain tissue do not correlate with these findings. In these studies, concentrations of Aβ$_{40}$ are low with Aβ$_{42}$ often identified as the dominant species. The data suggest preferential brain tissue utilisation and/or clearance of Aβ$_{40}$ compared with Aβ$_{42}$, findings which may have been predicted by their physiochemical differences. In Alzheimer’s disease this equilibrium is disrupted significantly increasing Aβ peptide levels in brain tissue. The disease-specific increase in Aβ$_{40}$ brain tissue levels in Alzheimer’s disease appears to be an important though overlooked pathological change compared with the welldocumented Aβ$_{42}$ change observed both in the aged and in Alzheimer’s disease. These findings are discussed in association with Aβ peptide function and a model of toxicity developed.
Starting Page	29
Ending Page	41
Page Count	13
File Format	PDF
ISSN	10298428
Journal	Neurotoxicity Research
Volume Number	7
Issue Number	1-2
e-ISSN	14763524
Language	English
Publisher	Springer-Verlag
Publisher Date	2005-01-01
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Beta amyloid peptide Aβ alloforms Secretases Alzheimer disease Neurosciences Pharmaceutical Sciences/Technology Neurology Neurochemistry Pharmacology/Toxicology Neurobiology
Content Type	Text
Resource Type	Article
Subject	Neuroscience Toxicology

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