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@ARTICLE{Minoshima:916863,
author = {Minoshima, Satoshi and Cross, Donna and Thientunyakit,
Tanyaluck and Foster, Norman L. and Drzezga, Alexander},
title = {18 {F}-{FDG} {PET} {I}maging in {N}eurodegenerative
{D}ementing {D}isorders: {I}nsights into {S}ubtype
{C}lassification, {E}merging {D}isease {C}ategories, and
{M}ixed {D}ementia with {C}opathologies},
journal = {Journal of nuclear medicine},
volume = {63},
number = {Supplement 1},
issn = {0097-9058},
address = {New York, NY},
publisher = {Soc.},
reportid = {FZJ-2023-00155},
pages = {2S - 12S},
year = {2022},
abstract = {Since the invention of 18F-FDG as a neurochemical tracer in
the 1970s, 18F-FDG PET has been used extensively for
dementia research and clinical applications. FDG, a glucose
analog, is transported into the brain via glucose
transporters and metabolized in a concerted process
involving astrocytes and neurons. Although the exact
cellular mechanisms of glucose consumption are still under
investigation, 18F-FDG PET can sensitively detect altered
neuronal activity due to neurodegeneration. Various
neurodegenerative disorders affect different areas of the
brain, which can be depicted as altered 18F-FDG uptake by
PET. The spatial patterns and severity of such changes can
be reproducibly visualized by statistical mapping
technology, which has become widely available in the clinic.
The differentiation of 3 major neurodegenerative disorders
by 18F-FDG PET, Alzheimer disease (AD), frontotemporal
dementia (FTD), and dementia with Lewy bodies (DLB), has
become standard practice. As the nosology of FTD evolves,
frontotemporal lobar degeneration, the umbrella term for
pathology affecting the frontal and temporal lobes, has been
subclassified clinically into behavioral variant FTD;
primary progressive aphasia with 3 subtypes, semantic,
nonfluent, and logopenic variants; and movement disorders
including progressive supranuclear palsy and corticobasal
degeneration. Each of these subtypes is associated with
differential 18F-FDG PET findings. The discovery of new
pathologic markers and clinicopathologic correlations via
larger autopsy series have led to newly recognized or
redefined disease categories, such as limbic-predominant
age-related TDP-43 encephalopathy, hippocampus sclerosis,
primary age-related tauopathy, and argyrophilic grain
disease, which have become a focus of investigations by
molecular imaging. These findings need to be integrated into
the modern interpretation of 18F-FDG PET. Recent pathologic
investigations also have revealed a high prevalence,
particularly in the elderly, of mixed dementia with
overlapping and coexisting pathologies. The interpretation
of 18F-FDG PET is evolving from a traditional dichotomous
diagnosis of AD versus FTD (or DLB) to a determination of
the most predominant underlying pathology that would best
explain the patient's symptoms, for the purpose of care
guidance. 18F-FDG PET is a relatively low cost and widely
available imaging modality that can help assess various
neurodegenerative disorders in a single test and remains the
workhorse in clinical dementia evaluation.},
cin = {INM-2},
ddc = {610},
cid = {I:(DE-Juel1)INM-2-20090406},
pnm = {5253 - Neuroimaging (POF4-525)},
pid = {G:(DE-HGF)POF4-5253},
typ = {PUB:(DE-HGF)16},
pubmed = {35649653},
UT = {WOS:000807305900002},
doi = {10.2967/jnumed.121.263194},
url = {https://juser.fz-juelich.de/record/916863},
}