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The molecular pathology of Alzheimer's disease.
Neuroimaging Clin N Am. 2012 Feb; 22(1):11-22, vii.NC

Abstract

Neurofibrillary pathology in Alzheimer's disease consists of paired helical filaments comprising tau protein. This pathology is correlated with dementia, but can appear in the first two decades of life. Extracellular amyloid β-protein arises through proteolytic processing of a transmembrane precursor, which involves the action of several enzymes. Mutations in the genes for the precursor and presenilin proteins accelerate the deposition of Aβ. Tau mutations cause other tauopathies in the absence of amyloid deposition, indicating that amyloid deposition is not a prerequisite for dementia. An improved understanding of Alzheimer's disease awaits to be obtained by molecular imaging of these pathologies.

Authors+Show Affiliations

Division of Applied Health Sciences, School of Medicine and Dentistry, Institute of Medical Sciences, University of Aberdeen, Liberty Building, Foresterhill Road, Aberdeen AB25 2ZP, Scotland, UK. c.harrington@abdn.ac.uk

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

22284730

Citation

Harrington, Charles R.. "The Molecular Pathology of Alzheimer's Disease." Neuroimaging Clinics of North America, vol. 22, no. 1, 2012, pp. 11-22, vii.
Harrington CR. The molecular pathology of Alzheimer's disease. Neuroimaging Clin N Am. 2012;22(1):11-22, vii.
Harrington, C. R. (2012). The molecular pathology of Alzheimer's disease. Neuroimaging Clinics of North America, 22(1), 11-22, vii. https://doi.org/10.1016/j.nic.2011.11.003
Harrington CR. The Molecular Pathology of Alzheimer's Disease. Neuroimaging Clin N Am. 2012;22(1):11-22, vii. PubMed PMID: 22284730.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The molecular pathology of Alzheimer's disease. A1 - Harrington,Charles R, PY - 2012/1/31/entrez PY - 2012/1/31/pubmed PY - 2012/5/30/medline SP - 11-22, vii JF - Neuroimaging clinics of North America JO - Neuroimaging Clin N Am VL - 22 IS - 1 N2 - Neurofibrillary pathology in Alzheimer's disease consists of paired helical filaments comprising tau protein. This pathology is correlated with dementia, but can appear in the first two decades of life. Extracellular amyloid β-protein arises through proteolytic processing of a transmembrane precursor, which involves the action of several enzymes. Mutations in the genes for the precursor and presenilin proteins accelerate the deposition of Aβ. Tau mutations cause other tauopathies in the absence of amyloid deposition, indicating that amyloid deposition is not a prerequisite for dementia. An improved understanding of Alzheimer's disease awaits to be obtained by molecular imaging of these pathologies. SN - 1557-9867 UR - https://www.unboundmedicine.com/medline/citation/22284730/The_molecular_pathology_of_Alzheimer's_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1052-5149(11)00173-0 DB - PRIME DP - Unbound Medicine ER -