Traumatic Brain Injury, Chronic Traumatic Encephalopathy, and Alzheimer's Disease: Common Pathologies Potentiated by Altered Zinc Homeostasis

Stuart D. Portbury; Paul A. Adlard

doi:10.3233/AIAD200024

Traumatic Brain Injury, Chronic Traumatic Encephalopathy, and Alzheimer's Disease: Common Pathologies Potentiated by Altered Zinc Homeostasis

Stuart D. Portbury
, Paul A. Adlard

Research output: Chapter in Book/Report/Conference proceeding › Chapter › peer-review

Abstract

Alzheimer's disease, traumatic brain injury, and chronic traumatic encephalopathy represent conditions that have a profound socioeconomic impact for both the individual and the wider community. They are all characterized by specific protein aggregation that results in synaptic dysfunction, neuronal death, and consequent cognitive decline and memory loss. In this review, we present evidence to support the notion that the common pathologies found in all conditions, and indeed their associated cognitive deficits, may be linked by zinc (Zn²⁺) ion dyshomeostasis. Elucidation of this hypothesis may present new therapeutic avenues for these devastating conditions.

Original language	English
Title of host publication	Handbook of Traumatic Brain Injury and Neurodegeneration
Editors	Rudy J. Castellani
Publisher	IOS Press
Pages	329-343
Number of pages	15
ISBN (Electronic)	9781643680644
DOIs	https://doi.org/10.3233/AIAD200024
State	Published - 2020
Externally published	Yes

Publication series

Name	Advances in Alzheimer's Disease
Volume	7
ISSN (Print)	2210-5727
ISSN (Electronic)	2210-5735

Keywords

Alzheimer's disease
TDP-43
amyloid-β
brain injury
cognition
tau protein
zinc

Access to Document

10.3233/AIAD200024

Cite this

Portbury, S. D., & Adlard, P. A. (2020). Traumatic Brain Injury, Chronic Traumatic Encephalopathy, and Alzheimer's Disease: Common Pathologies Potentiated by Altered Zinc Homeostasis. In R. J. Castellani (Ed.), Handbook of Traumatic Brain Injury and Neurodegeneration (pp. 329-343). (Advances in Alzheimer's Disease; Vol. 7). IOS Press. https://doi.org/10.3233/AIAD200024

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abstract = "Alzheimer's disease, traumatic brain injury, and chronic traumatic encephalopathy represent conditions that have a profound socioeconomic impact for both the individual and the wider community. They are all characterized by specific protein aggregation that results in synaptic dysfunction, neuronal death, and consequent cognitive decline and memory loss. In this review, we present evidence to support the notion that the common pathologies found in all conditions, and indeed their associated cognitive deficits, may be linked by zinc (Zn2+) ion dyshomeostasis. Elucidation of this hypothesis may present new therapeutic avenues for these devastating conditions.",

keywords = "Alzheimer's disease, TDP-43, amyloid-β, brain injury, cognition, tau protein, zinc",

author = "Portbury, \{Stuart D.\} and Adlard, \{Paul A.\}",

year = "2020",

doi = "10.3233/AIAD200024",

language = "English",

series = "Advances in Alzheimer's Disease",

publisher = "IOS Press",

pages = "329--343",

editor = "Castellani, \{Rudy J.\}",

booktitle = "Handbook of Traumatic Brain Injury and Neurodegeneration",

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}

Traumatic Brain Injury, Chronic Traumatic Encephalopathy, and Alzheimer's Disease: Common Pathologies Potentiated by Altered Zinc Homeostasis. / Portbury, Stuart D.; Adlard, Paul A.
Handbook of Traumatic Brain Injury and Neurodegeneration. ed. / Rudy J. Castellani. IOS Press, 2020. p. 329-343 (Advances in Alzheimer's Disease; Vol. 7).

Research output: Chapter in Book/Report/Conference proceeding › Chapter › peer-review

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AU - Adlard, Paul A.

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Y1 - 2020

N2 - Alzheimer's disease, traumatic brain injury, and chronic traumatic encephalopathy represent conditions that have a profound socioeconomic impact for both the individual and the wider community. They are all characterized by specific protein aggregation that results in synaptic dysfunction, neuronal death, and consequent cognitive decline and memory loss. In this review, we present evidence to support the notion that the common pathologies found in all conditions, and indeed their associated cognitive deficits, may be linked by zinc (Zn2+) ion dyshomeostasis. Elucidation of this hypothesis may present new therapeutic avenues for these devastating conditions.

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KW - brain injury

KW - cognition

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ER -

Traumatic Brain Injury, Chronic Traumatic Encephalopathy, and Alzheimer's Disease: Common Pathologies Potentiated by Altered Zinc Homeostasis

Abstract

Publication series

Keywords

Access to Document

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Cite this