In Alzheimer's disease, amyloid beta accumulation is a protective mechanism that ultimately fails
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In Alzheimer's disease, amyloid beta accumulation is a protective mechanism that ultimately fails. / Rischel, Elise Brøchner; Gejl, Michael; Brock, Birgitte; Rungby, Jørgen; Gjedde, Albert.
In: Alzheimer's and Dementia, Vol. 19, No. 3, 2023, p. 771–783.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - In Alzheimer's disease, amyloid beta accumulation is a protective mechanism that ultimately fails
AU - Rischel, Elise Brøchner
AU - Gejl, Michael
AU - Brock, Birgitte
AU - Rungby, Jørgen
AU - Gjedde, Albert
N1 - Publisher Copyright: © 2022 The Authors. Alzheimer's & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer's Association.
PY - 2023
Y1 - 2023
N2 - Hypothesis and predictions: Here, we claim that amyloid beta (Aβ) accumulation is a protective mechanism that ultimately fails. We predict that more Aβ accumulates in regions with higher rates of glucose metabolism, reaching a maximum followed by progression of pathology. Background: Aβ accumulation is characteristic of Alzheimer's disease (AD) but the accumulation does not correlate with cognitive decline, unlike the rates of glucose metabolism. Strategy: We compared averaged and individual estimates of regional binding potentials of [11C]Pittsburgh compound B to regionally averaged and individual values of metabolism of [18F]fluorodeoxyglucose in brain regions of volunteers with AD. Significance: The claim explains the cognitive decline in some patients at a significantly lower level of Aβ deposition than in other patients, as well as the presence of cognitively healthy individuals with high Aβ accumulation. With further support of the hypothesis, the significance of Aβ accumulation in brains of patients with AD may require revision.
AB - Hypothesis and predictions: Here, we claim that amyloid beta (Aβ) accumulation is a protective mechanism that ultimately fails. We predict that more Aβ accumulates in regions with higher rates of glucose metabolism, reaching a maximum followed by progression of pathology. Background: Aβ accumulation is characteristic of Alzheimer's disease (AD) but the accumulation does not correlate with cognitive decline, unlike the rates of glucose metabolism. Strategy: We compared averaged and individual estimates of regional binding potentials of [11C]Pittsburgh compound B to regionally averaged and individual values of metabolism of [18F]fluorodeoxyglucose in brain regions of volunteers with AD. Significance: The claim explains the cognitive decline in some patients at a significantly lower level of Aβ deposition than in other patients, as well as the presence of cognitively healthy individuals with high Aβ accumulation. With further support of the hypothesis, the significance of Aβ accumulation in brains of patients with AD may require revision.
KW - Alzheimer's disease
KW - amyloid beta
KW - blood–brain barrier
KW - cerebral blood flow
KW - cerebral glucose metabolism
KW - positron emission tomography
KW - [C]Pittsburgh compound B
KW - [F]fluorodeoxyglucose
U2 - 10.1002/alz.12701
DO - 10.1002/alz.12701
M3 - Journal article
C2 - 35673950
AN - SCOPUS:85131333087
VL - 19
SP - 771
EP - 783
JO - Alzheimer's & Dementia
JF - Alzheimer's & Dementia
SN - 1552-5260
IS - 3
ER -
ID: 310377796