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.
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Publisher Full Text
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 -