Mapping biochemistry to metabolism: FDG-PET and amyloid burden in Alzheimer's disease

Michael S. Mega; Teresa Chu; John C. Mazziotta; Kashyap H. Trivedi; Paul M. Thompson; Amish Shah; Gregory Cole; Sally A. Frautschy; Arthur W. Toga

doi:10.1097/00001756-199909290-00007

Mapping biochemistry to metabolism: FDG-PET and amyloid burden in Alzheimer's disease

Michael S. Mega
, Teresa Chu
, John C. Mazziotta
, Kashyap H. Trivedi
, Paul M. Thompson
, Amish Shah
, Gregory Cole
, Sally A. Frautschy
, Arthur W. Toga

Research output: Contribution to journal › Article › peer-review

46 Scopus citations

Abstract

We evaluated the relationship between amyloid-β protein (Aβ) concentration and the metabolic abnormality in an Alzheimer's disease (AD) patient as measured by [¹⁸F]fluorodeoxyglucose positron emission tomography (FDG-PET). Across most regions there were significant inverse correlations among FDG-PET intensity values and both insoluble. The temporal lobe samples showed no significant correlation between FDG-PET values and Aβ deposition. Findings support Aβ as contributing to the hypometabolism in regions of the AD brain that are still relatively viable metabolically; those regions with chronic pathologic damage, such as temporal cortex, may have other factors that contribute to metabolic deficits.

Original language	English
Pages (from-to)	2911-2917
Number of pages	7
Journal	NeuroReport
Volume	10
Issue number	14
DOIs	https://doi.org/10.1097/00001756-199909290-00007
State	Published - 29 Sep 1999
Externally published	Yes

Keywords

Alzheimer's disease
Amyloid protein
Brain mapping
PET

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10.1097/00001756-199909290-00007

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title = "Mapping biochemistry to metabolism: FDG-PET and amyloid burden in Alzheimer's disease",

abstract = "We evaluated the relationship between amyloid-β protein (Aβ) concentration and the metabolic abnormality in an Alzheimer's disease (AD) patient as measured by [18F]fluorodeoxyglucose positron emission tomography (FDG-PET). Across most regions there were significant inverse correlations among FDG-PET intensity values and both insoluble. The temporal lobe samples showed no significant correlation between FDG-PET values and Aβ deposition. Findings support Aβ as contributing to the hypometabolism in regions of the AD brain that are still relatively viable metabolically; those regions with chronic pathologic damage, such as temporal cortex, may have other factors that contribute to metabolic deficits.",

keywords = "Alzheimer's disease, Amyloid protein, Brain mapping, PET",

author = "Mega, \{Michael S.\} and Teresa Chu and Mazziotta, \{John C.\} and Trivedi, \{Kashyap H.\} and Thompson, \{Paul M.\} and Amish Shah and Gregory Cole and Frautschy, \{Sally A.\} and Toga, \{Arthur W.\}",

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T2 - FDG-PET and amyloid burden in Alzheimer's disease

AU - Mega, Michael S.

AU - Chu, Teresa

AU - Mazziotta, John C.

AU - Trivedi, Kashyap H.

AU - Thompson, Paul M.

AU - Shah, Amish

AU - Cole, Gregory

AU - Frautschy, Sally A.

AU - Toga, Arthur W.

PY - 1999/9/29

Y1 - 1999/9/29

N2 - We evaluated the relationship between amyloid-β protein (Aβ) concentration and the metabolic abnormality in an Alzheimer's disease (AD) patient as measured by [18F]fluorodeoxyglucose positron emission tomography (FDG-PET). Across most regions there were significant inverse correlations among FDG-PET intensity values and both insoluble. The temporal lobe samples showed no significant correlation between FDG-PET values and Aβ deposition. Findings support Aβ as contributing to the hypometabolism in regions of the AD brain that are still relatively viable metabolically; those regions with chronic pathologic damage, such as temporal cortex, may have other factors that contribute to metabolic deficits.

AB - We evaluated the relationship between amyloid-β protein (Aβ) concentration and the metabolic abnormality in an Alzheimer's disease (AD) patient as measured by [18F]fluorodeoxyglucose positron emission tomography (FDG-PET). Across most regions there were significant inverse correlations among FDG-PET intensity values and both insoluble. The temporal lobe samples showed no significant correlation between FDG-PET values and Aβ deposition. Findings support Aβ as contributing to the hypometabolism in regions of the AD brain that are still relatively viable metabolically; those regions with chronic pathologic damage, such as temporal cortex, may have other factors that contribute to metabolic deficits.

KW - Alzheimer's disease

KW - Amyloid protein

KW - Brain mapping

KW - PET

UR - https://www.scopus.com/pages/publications/0033615219

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Mapping biochemistry to metabolism: FDG-PET and amyloid burden in Alzheimer's disease

Abstract

Keywords

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