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46/100

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Brain scans and imaging

Topic: Brain proteins, microglia and lab models

Unlabelled Amyloid imaging by small-animal PET in models of Alzheimer disease (AD) offers the possibility to track amyloidogenesis and brain energy metabolism. Because microglial activation is thought to contribute to AD pathology, we undertook a triple-tracer small-animal PET study to assess microglial activation and glucose metabolism in association with amyloid plaque load in a transgenic AD mouse model. Methods Groups of PS2APP and C57BL/6 wild-type mice of various ages were examined by small-animal PET. We acquired 90-min dynamic emission data with (18)F-GE180 for imaging activated microglia (18-kD translocator protein ligand [TSPO]) and static 30- to 60-min recordings with (18)F-FDG for energy metabolism and (18)F-florbetaben for amyloidosis. Optimal fusion of PET data was obtained through automatic nonlinear spatial normalization, and SUVRs were calculated. For the novel TSPO tracer (18)F-GE180, we then calculated distribution volume ratios after establishing a suitable reference region. Immunohistochemical analyses with TSPO antisera, methoxy-X04 staining for fibrillary β-amyloid, and ex vivo autoradiography served as terminal gold standard assessments. Results SUVR at 60-90 min after injection gave robust quantitation of (18)F-GE180, which correlated well with distribution volume ratios calculated from the entire recording and using a white matter reference region. Relative to age-matched wild-type, (18)F-GE180 SUVR was slightly elevated in PS2APP mice at 5 mo (+9%; P Conclusion In this first triple-tracer small-animal PET in a well-established AD mouse model, we found evidence for age-dependent microglial activation. This activation, correlating positively with the amyloid load, implies a relationship between amyloidosis and inflammation in the PS2APP AD mouse model.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Brendel, M., Probst, F., Jaworska, A., Overhoff, F., Korzhova, V., Albert, N. L., et al. (2016). Glial Activation and Glucose Metabolism in a Transgenic Amyloid Mouse Model: A Triple-Tracer PET Study. Journal of nuclear medicine : official publication, Society of Nuclear Medicine. https://doi.org/10.2967/jnumed.115.167858

Vancouver

Brendel M, Probst F, Jaworska A, Overhoff F, Korzhova V, Albert NL, et al. Glial Activation and Glucose Metabolism in a Transgenic Amyloid Mouse Model: A Triple-Tracer PET Study. Journal of nuclear medicine : official publication, Society of Nuclear Medicine. 2016. doi:10.2967/jnumed.115.167858. PMID: 26912428.

BibTeX

@article{brendel2016-26912428,
  author  = {Brendel, M. and Probst, F. and Jaworska, A. and Overhoff, F. and Korzhova, V. and Albert, N. L. and Beck, R. and Lindner, S. and others},
  title   = {{Glial Activation and Glucose Metabolism in a Transgenic Amyloid Mouse Model: A Triple-Tracer PET Study}},
  journal = {Journal of nuclear medicine : official publication, Society of Nuclear Medicine},
  year    = {2016},
  doi     = {10.2967/jnumed.115.167858},
  pmid    = {26912428},
  url     = {https://doi.org/10.2967/jnumed.115.167858}
}

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Key findings

Results SUVR at 60-90 min after injection gave robust quantitation of (18)F-GE180, which correlated well with distribution volume ratios calculated from the entire recording and using a white matter reference region.
Relative to age-matched wild-type, (18)F-GE180 SUVR was slightly elevated in PS2APP mice at 5 mo (+9%; P Conclusion In this first triple-tracer small-animal PET in a well-established AD mouse model, we found evidence for age-dependent microglial activation.

Why it matters

In a mouse model of Alzheimer-like amyloid, PET showed age-dependent microglial activation along with amyloid and metabolic changes. These are animal findings and do not establish any treatment or prevention for people.

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Study details

Evidence strengthLow

How this study scored 46/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomized / blinded because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Journal of nuclear medicine : official publication, Society of Nuclear Medicine)
Journal's citation record	2 / 4	Journal of Nuclear Medicine: journal h-index 230 (OpenAlex, 2026-10-29)
Study design	0 / 12	No study design recorded — scores zero, not guessed (not stated in the record — scored 0)
Strength of evidence	1 / 5	Rated “low” in our summary
Peer-review validation	10 / 10	Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent	1 / 5	2016 — within 20 year(s) of the newest study here
Sample size	0 / 4	Participant count not stated — scores zero (not stated in the record — scored 0)
Effect reported	0 / 3	No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people	0 / 3	Laboratory or animal study (title names “transgenic”) — scores zero
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	5 / 7	Cited 145 times (OpenAlex, 2026-10-10)
Citations per year	3 / 5	12.1 citations a year over 12 year(s) since 2016
Impact for its field and year	4 / 6	Cited 11.4× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	3 / 6	Cited by 14 other studies in this library
Still being cited	2 / 4	Cited 34 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	3 / 4	Last-listed author Axel Rominger: h-index 54 (OpenAlex, whole career)
Institution's track record	1 / 3	Ludwig-Maximilians-Universität München: institution h-index 1,224 (OpenAlex)
Multicenter collaboration	2 / 3	OpenAlex lists 4 institution(s) in 2 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 26912428)
Free to read	0 / 2	Behind a paywall — scores zero
Total	46 / 100	—

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