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Accumulated amyloid-beta peptide and hyperphosphorylated tau protein: relationship and links in Alzheimer's disease.
J Alzheimers Dis. 2009; 16(1):15-27.JA

Abstract

The neuropathology associated with Alzheimer's disease (AD) is characterized by the presence of extracellularly neuritic plaques, intracellularly neurofibrillary tangles and the loss of basal forebrain cholinergic neurons. The neuritic plaque is composed of a core of amyloid-beta peptide (Abeta) while the neurofibrillary tangles contain phosphorylated tau protein, and, as such, both Abeta and tau are important molecules associated with AD. In healthy human bodies, clearance mechanisms for Abeta are available; yet if clearance fails, Abeta accumulates, increasing the risk of neurotoxicity in the brain. Tau, one of the main microtubule-associated proteins, will be hyperphosphorylated and lose the ability to bind microtubules when the homeostasis of phosphorylation and dephosphorylation is disturbed in neurons. Accumulated Abeta and hyperphosphorylated tau are thought to be coexistent. Research on the pathological changes in AD indicates that accumulated Abeta in vivo may initiate the hyperphosphorylation of tau. Also, the signal transduction pathways of tau hyperphosphorylation may be related to accumulated Abeta. In this review, we will discuss how Abeta accumulates, how tau protein is hyperphosphorylated, and how accumulated Abeta initiates hyperphosphorylation of tau protein in AD.

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Authors+Show Affiliations

Huang HC
Beijing Union University, Beijing, China. hanchang@ygi.edu.cn
Jiang ZF
No affiliation info available

MeSH

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsHumansPhosphorylationSignal Transductiontau Proteins

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

19158417

Citation

Huang, Han-Chang, and Zhao-Feng Jiang. "Accumulated Amyloid-beta Peptide and Hyperphosphorylated Tau Protein: Relationship and Links in Alzheimer's Disease." Journal of Alzheimer's Disease : JAD, vol. 16, no. 1, 2009, pp. 15-27.
Huang HC, Jiang ZF. Accumulated amyloid-beta peptide and hyperphosphorylated tau protein: relationship and links in Alzheimer's disease. J Alzheimers Dis. 2009;16(1):15-27.
Huang, H. C., & Jiang, Z. F. (2009). Accumulated amyloid-beta peptide and hyperphosphorylated tau protein: relationship and links in Alzheimer's disease. Journal of Alzheimer's Disease : JAD, 16(1), 15-27. https://doi.org/10.3233/JAD-2009-0960
Huang HC, Jiang ZF. Accumulated Amyloid-beta Peptide and Hyperphosphorylated Tau Protein: Relationship and Links in Alzheimer's Disease. J Alzheimers Dis. 2009;16(1):15-27. PubMed PMID: 19158417.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Accumulated amyloid-beta peptide and hyperphosphorylated tau protein: relationship and links in Alzheimer's disease. AU - Huang,Han-Chang, AU - Jiang,Zhao-Feng, PY - 2009/1/23/entrez PY - 2009/1/23/pubmed PY - 2009/3/28/medline SP - 15 EP - 27 JF - Journal of Alzheimer's disease : JAD JO - J Alzheimers Dis VL - 16 IS - 1 N2 - The neuropathology associated with Alzheimer's disease (AD) is characterized by the presence of extracellularly neuritic plaques, intracellularly neurofibrillary tangles and the loss of basal forebrain cholinergic neurons. The neuritic plaque is composed of a core of amyloid-beta peptide (Abeta) while the neurofibrillary tangles contain phosphorylated tau protein, and, as such, both Abeta and tau are important molecules associated with AD. In healthy human bodies, clearance mechanisms for Abeta are available; yet if clearance fails, Abeta accumulates, increasing the risk of neurotoxicity in the brain. Tau, one of the main microtubule-associated proteins, will be hyperphosphorylated and lose the ability to bind microtubules when the homeostasis of phosphorylation and dephosphorylation is disturbed in neurons. Accumulated Abeta and hyperphosphorylated tau are thought to be coexistent. Research on the pathological changes in AD indicates that accumulated Abeta in vivo may initiate the hyperphosphorylation of tau. Also, the signal transduction pathways of tau hyperphosphorylation may be related to accumulated Abeta. In this review, we will discuss how Abeta accumulates, how tau protein is hyperphosphorylated, and how accumulated Abeta initiates hyperphosphorylation of tau protein in AD. SN - 1387-2877 UR - https://www.unboundmedicine.com/medline/citation/19158417/Accumulated_amyloid_beta_peptide_and_hyperphosphorylated_tau_protein:_relationship_and_links_in_Alzheimer's_disease_ L2 - https://content.iospress.com/openurl?genre=article&issn=1387-2877&volume=16&issue=1&spage=15 DB - PRIME DP - Unbound Medicine ER -