Moving away from amyloid beta to move on in Alzheimer research

María G. Moreno-Treviño, Jesús Castillo-López, Irene Meester

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

© 2015 Moreno-Treviño, Castillo-López and Meester. Alzheimer's disease (AD) is characterized by a progressive decay of cognitive abilities, most remarkably (spatial) memory and learning. AD is diagnosed by clinical mental tests, often combined with the detection of neurobiological markers, mainly brain imaging studies and a decreased amyloid beta (Aß) level and/or increased total and hyper-phosphorylated Tau protein (tau-P) in cerebral spinal fluid (Hampel et al., 2008; Alzheimer's Association, 2014). The diagnosis is confirmed post-mortem by histopathological detection of senile plaques, composed of Aß accumulations, and tau-P-containing neurofibrillary tangles (Jellinger and Bancher, 1998). However, non-demented, aged patients may have a histopathology that is indistinguishable from AD (Price and Morris, 1999; Nelson et al., 2012). Furthermore, the brains of AD may have additional changes, such as (micro)vascular changes (Scheibel et al., 1989; de la Torre, 2002; Bell and Zlokovic, 2009; Hommet et al., 2011), white matter hyperintensities (Kandiah et al., 2015), and vacuolar cells, which are not considered as pathognomonic features under current standards (Nelson et al., 2012).
Original languageEnglish
JournalFrontiers in Aging Neuroscience
DOIs
Publication statusPublished - 1 Jan 2015

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Amyloid
Alzheimer Disease
tau Proteins
Research
Neurofibrillary Tangles
Intelligence Tests
Aptitude
Amyloid Plaques
Brain Diseases
Neuroimaging
Blood Vessels

All Science Journal Classification (ASJC) codes

  • Ageing
  • Cognitive Neuroscience

Cite this

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title = "Moving away from amyloid beta to move on in Alzheimer research",
abstract = "{\circledC} 2015 Moreno-Trevi{\~n}o, Castillo-L{\'o}pez and Meester. Alzheimer's disease (AD) is characterized by a progressive decay of cognitive abilities, most remarkably (spatial) memory and learning. AD is diagnosed by clinical mental tests, often combined with the detection of neurobiological markers, mainly brain imaging studies and a decreased amyloid beta (A{\ss}) level and/or increased total and hyper-phosphorylated Tau protein (tau-P) in cerebral spinal fluid (Hampel et al., 2008; Alzheimer's Association, 2014). The diagnosis is confirmed post-mortem by histopathological detection of senile plaques, composed of A{\ss} accumulations, and tau-P-containing neurofibrillary tangles (Jellinger and Bancher, 1998). However, non-demented, aged patients may have a histopathology that is indistinguishable from AD (Price and Morris, 1999; Nelson et al., 2012). Furthermore, the brains of AD may have additional changes, such as (micro)vascular changes (Scheibel et al., 1989; de la Torre, 2002; Bell and Zlokovic, 2009; Hommet et al., 2011), white matter hyperintensities (Kandiah et al., 2015), and vacuolar cells, which are not considered as pathognomonic features under current standards (Nelson et al., 2012).",
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Moving away from amyloid beta to move on in Alzheimer research. / Moreno-Treviño, María G.; Castillo-López, Jesús; Meester, Irene.

In: Frontiers in Aging Neuroscience, 01.01.2015.

Research output: Contribution to journalArticle

TY - JOUR

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AB - © 2015 Moreno-Treviño, Castillo-López and Meester. Alzheimer's disease (AD) is characterized by a progressive decay of cognitive abilities, most remarkably (spatial) memory and learning. AD is diagnosed by clinical mental tests, often combined with the detection of neurobiological markers, mainly brain imaging studies and a decreased amyloid beta (Aß) level and/or increased total and hyper-phosphorylated Tau protein (tau-P) in cerebral spinal fluid (Hampel et al., 2008; Alzheimer's Association, 2014). The diagnosis is confirmed post-mortem by histopathological detection of senile plaques, composed of Aß accumulations, and tau-P-containing neurofibrillary tangles (Jellinger and Bancher, 1998). However, non-demented, aged patients may have a histopathology that is indistinguishable from AD (Price and Morris, 1999; Nelson et al., 2012). Furthermore, the brains of AD may have additional changes, such as (micro)vascular changes (Scheibel et al., 1989; de la Torre, 2002; Bell and Zlokovic, 2009; Hommet et al., 2011), white matter hyperintensities (Kandiah et al., 2015), and vacuolar cells, which are not considered as pathognomonic features under current standards (Nelson et al., 2012).

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