Neuropathological correlates of amyloid PET imaging in Down syndrome

Down syndrome (DS) results in an overproduction of amyloid‐β (Aβ) peptide associated with early onset of Alzheimer's disease (AD). DS cases have Aβ deposits detectable histologically as young as 12–30 years of age, primarily in the form of diffuse plaques, the type of early amyloid pathology al...

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Published inDevelopmental neurobiology (Hoboken, N.J.) Vol. 79; no. 7; pp. 750 - 766
Main Authors Abrahamson, Eric E., Head, Elizabeth, Lott, Ira T., Handen, Benjamin L., Mufson, Elliott J., Christian, Bradley T., Klunk, William E., Ikonomovic, Milos D.
Format Journal Article
LanguageEnglish
Published United States Wiley Subscription Services, Inc 01.07.2019
Subjects
Aging
Alzheimer's disease
amyloid
Amyloid beta-Peptides - metabolism
Animals
Autopsy
Axons
Brain - diagnostic imaging
Brain - metabolism
Cortex
Dementia disorders
Down syndrome
Down Syndrome - diagnostic imaging
Down Syndrome - metabolism
Down's syndrome
Humans
Neurodegenerative diseases
Neuroimaging
Neuropathology
Pathology
Positron emission tomography
Positron-Emission Tomography - methods
Senile plaques
striatum
β-Amyloid
amyloid
Down syndrome
striatum
positron emission tomography
Alzheimer's disease
neuropathology
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Abstract Down syndrome (DS) results in an overproduction of amyloid‐β (Aβ) peptide associated with early onset of Alzheimer's disease (AD). DS cases have Aβ deposits detectable histologically as young as 12–30 years of age, primarily in the form of diffuse plaques, the type of early amyloid pathology also seen at pre‐clinical (i.e., pathological aging) and prodromal stages of sporadic late onset AD. In DS subjects aged >40 years, levels of cortical Aβ deposition are similar to those observed in late onset AD and in addition to diffuse plaques involve cored plaques associated with dystrophic neurites (neuritic plaques), which are of neuropathological diagnostic significance in AD. The purpose of this review is to summarize and discuss findings from amyloid PET imaging studies of DS in reference to postmortem amyloid‐based neuropathology. PET neuroimaging applied to subjects with DS has the potential to (a) track the natural progression of brain pathology, including the earliest stages of amyloid accumulation, and (b) determine whether amyloid PET biomarkers predict the onset of dementia. In addition, the question that is still incompletely understood and relevant to both applications is the ability of amyloid PET to detect Aβ deposits in their earliest form.
AbstractList Down syndrome (DS) results in an over-production of amyloid-β (Aβ) peptide associated with early onset of Alzheimer’s disease (AD). DS cases have Aβ deposits detectable histologically as young as 12–30 years of age, primarily in the form of diffuse plaques, the type of early amyloid pathology also seen at pre-clinical (i.e., pathological aging) and prodromal stages of sporadic late onset AD. In DS subjects aged >40 years, levels of cortical Aβ deposition are similar to those observed in late onset AD and in addition to diffuse plaques involve cored plaques associated with dystrophic neurites (neuritic plaques) which are of neuropathological diagnostic significance in AD. The purpose of this review is to summarize and discuss findings from amyloid PET imaging studies of DS in reference to post-mortem amyloid based neuropathology. PET neuroimaging applied to subjects with DS has the potential to a) track the natural progression of brain pathology, including the earliest stages of amyloid accumulation, and b) determine whether amyloid PET biomarkers predict the onset of dementia. In addition, the question that is still incompletely understood and relevant to both applications is the ability of amyloid PET to detect Aβ deposits in their earliest form.
Down syndrome (DS) results in an overproduction of amyloid‐β (Aβ) peptide associated with early onset of Alzheimer's disease (AD). DS cases have Aβ deposits detectable histologically as young as 12–30 years of age, primarily in the form of diffuse plaques, the type of early amyloid pathology also seen at pre‐clinical (i.e., pathological aging) and prodromal stages of sporadic late onset AD. In DS subjects aged >40 years, levels of cortical Aβ deposition are similar to those observed in late onset AD and in addition to diffuse plaques involve cored plaques associated with dystrophic neurites (neuritic plaques), which are of neuropathological diagnostic significance in AD. The purpose of this review is to summarize and discuss findings from amyloid PET imaging studies of DS in reference to postmortem amyloid‐based neuropathology. PET neuroimaging applied to subjects with DS has the potential to (a) track the natural progression of brain pathology, including the earliest stages of amyloid accumulation, and (b) determine whether amyloid PET biomarkers predict the onset of dementia. In addition, the question that is still incompletely understood and relevant to both applications is the ability of amyloid PET to detect Aβ deposits in their earliest form.
Down syndrome (DS) results in an overproduction of amyloid‐β (Aβ) peptide associated with early onset of Alzheimer's disease (AD). DS cases have Aβ deposits detectable histologically as young as 12–30 years of age, primarily in the form of diffuse plaques, the type of early amyloid pathology also seen at pre‐clinical (i.e., pathological aging) and prodromal stages of sporadic late onset AD. In DS subjects aged >40 years, levels of cortical Aβ deposition are similar to those observed in late onset AD and in addition to diffuse plaques involve cored plaques associated with dystrophic neurites (neuritic plaques), which are of neuropathological diagnostic significance in AD. The purpose of this review is to summarize and discuss findings from amyloid PET imaging studies of DS in reference to postmortem amyloid‐based neuropathology. PET neuroimaging applied to subjects with DS has the potential to (a) track the natural progression of brain pathology, including the earliest stages of amyloid accumulation, and (b) determine whether amyloid PET biomarkers predict the onset of dementia. In addition, the question that is still incompletely understood and relevant to both applications is the ability of amyloid PET to detect Aβ deposits in their earliest form.
Down syndrome (DS) results in an overproduction of amyloid-β (Aβ) peptide associated with early onset of Alzheimer's disease (AD). DS cases have Aβ deposits detectable histologically as young as 12-30 years of age, primarily in the form of diffuse plaques, the type of early amyloid pathology also seen at pre-clinical (i.e., pathological aging) and prodromal stages of sporadic late onset AD. In DS subjects aged >40 years, levels of cortical Aβ deposition are similar to those observed in late onset AD and in addition to diffuse plaques involve cored plaques associated with dystrophic neurites (neuritic plaques), which are of neuropathological diagnostic significance in AD. The purpose of this review is to summarize and discuss findings from amyloid PET imaging studies of DS in reference to postmortem amyloid-based neuropathology. PET neuroimaging applied to subjects with DS has the potential to (a) track the natural progression of brain pathology, including the earliest stages of amyloid accumulation, and (b) determine whether amyloid PET biomarkers predict the onset of dementia. In addition, the question that is still incompletely understood and relevant to both applications is the ability of amyloid PET to detect Aβ deposits in their earliest form.Down syndrome (DS) results in an overproduction of amyloid-β (Aβ) peptide associated with early onset of Alzheimer's disease (AD). DS cases have Aβ deposits detectable histologically as young as 12-30 years of age, primarily in the form of diffuse plaques, the type of early amyloid pathology also seen at pre-clinical (i.e., pathological aging) and prodromal stages of sporadic late onset AD. In DS subjects aged >40 years, levels of cortical Aβ deposition are similar to those observed in late onset AD and in addition to diffuse plaques involve cored plaques associated with dystrophic neurites (neuritic plaques), which are of neuropathological diagnostic significance in AD. The purpose of this review is to summarize and discuss findings from amyloid PET imaging studies of DS in reference to postmortem amyloid-based neuropathology. PET neuroimaging applied to subjects with DS has the potential to (a) track the natural progression of brain pathology, including the earliest stages of amyloid accumulation, and (b) determine whether amyloid PET biomarkers predict the onset of dementia. In addition, the question that is still incompletely understood and relevant to both applications is the ability of amyloid PET to detect Aβ deposits in their earliest form.
Author Mufson, Elliott J.
Abrahamson, Eric E.
Lott, Ira T.
Christian, Bradley T.
Handen, Benjamin L.
Klunk, William E.
Head, Elizabeth
Ikonomovic, Milos D.
AuthorAffiliation 5 Department of Neurology, UC Irvine School of Medicine, Orange CA
2 Department of Neurology University of Pittsburgh, Pittsburgh PA
6 Department of Neurobiology, Barrow Neurological Institute, Phoenix AZ
3 Department of Psychiatry, University of Pittsburgh, Pittsburgh PA
7 Departments of Medical Physics and Psychiatry, Waisman Center, University of Wisconsin-Madison, Madison, WI
1 Geriatric Research Education and Clinical Center, VA Pittsburgh Healthcare System, University of Pittsburgh, Pittsburgh PA
4 Department of Pathology and Laboratory Medicine UC Irvine School of Medicine, Orange CA
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/31379087$$D View this record in MEDLINE/PubMed
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Keywords amyloid
Down syndrome
striatum
positron emission tomography
Alzheimer's disease
neuropathology
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wiley_primary_10_1002_dneu_22713_DNEU22713
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PublicationCentury 2000
PublicationDate July 2019
2019-07-00
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PublicationDateYYYYMMDD 2019-07-01
PublicationDate_xml – month: 07
  year: 2019
  text: July 2019
PublicationDecade 2010
PublicationPlace United States
PublicationPlace_xml – name: United States
– name: Hoboken
PublicationTitle Developmental neurobiology (Hoboken, N.J.)
PublicationTitleAlternate Dev Neurobiol
PublicationYear 2019
Publisher Wiley Subscription Services, Inc
Publisher_xml – name: Wiley Subscription Services, Inc
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Snippet Down syndrome (DS) results in an overproduction of amyloid‐β (Aβ) peptide associated with early onset of Alzheimer's disease (AD). DS cases have Aβ deposits...
Down syndrome (DS) results in an overproduction of amyloid-β (Aβ) peptide associated with early onset of Alzheimer's disease (AD). DS cases have Aβ deposits...
Down syndrome (DS) results in an over-production of amyloid-β (Aβ) peptide associated with early onset of Alzheimer’s disease (AD). DS cases have Aβ deposits...
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SubjectTerms Aging
Alzheimer's disease
amyloid
Amyloid beta-Peptides - metabolism
Animals
Autopsy
Axons
Brain - diagnostic imaging
Brain - metabolism
Cortex
Dementia disorders
Down syndrome
Down Syndrome - diagnostic imaging
Down Syndrome - metabolism
Down's syndrome
Humans
Neurodegenerative diseases
Neuroimaging
Neuropathology
Pathology
Positron emission tomography
Positron-Emission Tomography - methods
Senile plaques
striatum
β-Amyloid
Title Neuropathological correlates of amyloid PET imaging in Down syndrome
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fdneu.22713
https://www.ncbi.nlm.nih.gov/pubmed/31379087
https://www.proquest.com/docview/2295350445
https://www.proquest.com/docview/2268574537
https://pubmed.ncbi.nlm.nih.gov/PMC6892598
Volume 79
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