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47/100

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Mild cognitive impairment

Topic: Amyloid, tau and blood-test diagnosis

Background Alzheimer disease (AD) is defined neuropathologically by the presence of neurofibrillary tangles and plaques associated with tau and beta-amyloid protein deposition. The colocalization of microglia and beta-amyloid plaques has been widely reported in pathological examination of AD and suggests that neuroinflammation may play a role in pathogenesis and/or progression. Because postmortem histopathological analyses are limited to single end-stage assessment, the time course and nature of this relationship are not well understood. Objective To image microglial activation and beta-amyloid deposition in the brains of subjects with and without AD. Design, setting, and participants Using two carbon 11 ([11C])-labeled positron emission tomographic imaging agents, Pittsburgh Compound B (PiB) and (R)-PK11195, we examined the relationship between amyloid deposition and microglial activation in different stages of AD using 5 control subjects, 6 subjects diagnosed with mild cognitive impairment, and 6 patients with mild to moderate AD. Results Consistent with prior reports, subjects with a clinical diagnosis of probable AD showed significantly greater levels of [11C]PiB retention than control subjects, whereas patients with mild cognitive impairment spanned a range from control-like to AD-like levels of [11C]PiB retention. Additionally, 2 asymptomatic control subjects also exhibited evidence of elevated PiB retention in regions associated with the early emergence of plaques in AD and may represent prodromal cases of AD. We observed no differences in brain [11C](R)-PK11195 retention when subjects were grouped by clinical diagnosis or the presence or absence of beta-amyloid pathological findings as indicated by analyses of [11C]PiB retention. Conclusions These findings suggest that either microglial activation is limited to later stages of severe AD or [11C](R)-PK11195 is too insensitive to detect the level of microglial activation associated with mild to moderate AD.

Key findings

Background Alzheimer disease (AD) is defined neuropathologically by the presence of neurofibrillary tangles and plaques associated with tau and beta-amyloid protein deposition.
The colocalization of microglia and beta-amyloid plaques has been widely reported in pathological examination of AD and suggests that neuroinflammation may play a role in pathogenesis and/or progression.
Results Consistent with prior reports, subjects with a clinical diagnosis of probable AD showed significantly greater levels of [11C]PiB retention than control subjects, whereas patients with mild cognitive impairment spanned a range from control-like to AD-like levels of [11C]PiB retention.
Additionally, 2 asymptomatic control subjects also exhibited evidence of elevated PiB retention in regions associated with the early emergence of plaques in AD and may represent prodromal cases of AD.
We observed no differences in brain [11C](R)-PK11195 retention when subjects were grouped by clinical diagnosis or the presence or absence of beta-amyloid pathological findings as indicated by analyses of [11C]PiB retention.

Why it matters

Using PET imaging in a small number of subjects, probable Alzheimer's patients showed greater amyloid tracer retention than controls, while those with mild cognitive impairment ranged from control-like to Alzheimer-like levels. The study examined the relationship between amyloid deposition and microglial activation but did not test any treatment.

Study details

Evidence strengthLow

How this study scored 47/100

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

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Archives of neurology)
Journal's citation record	3 / 4	Archives of Neurology: journal h-index 353 (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	2009 — 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	Not stated whether this was studied in people — scores zero (not stated in the record — scored 0)
Randomised / blinded	0 / 2	No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	5 / 7	Cited 163 times (OpenAlex, 2026-10-10)
Citations per year	3 / 5	8.6 citations a year over 19 year(s) since 2009
Impact for its field and year	4 / 6	Cited 9.1× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	3 / 6	Cited by 20 other studies in this library
Still being cited	1 / 4	Cited 4 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	4 / 4	Last-listed author Chester A. Mathis: h-index 105 (OpenAlex, whole career)
Institution's track record	2 / 3	University of Pennsylvania: institution h-index 1,859 (OpenAlex)
Multi-centre collaboration	1 / 3	OpenAlex lists 2 institution(s) in 1 country
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 19139300)
Free to read	0 / 2	Behind a paywall — scores zero
Total	47 / 100	—

What each of these 20 components measures, and what this score is not →

Read the original

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

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.

APA 7th

Wiley, C. A., Lopresti, B. J., Venneti, S., Price, J., Klunk, W. E., DeKosky, S. T., et al. (2009). Carbon 11-labeled Pittsburgh Compound B and carbon 11-labeled (R)-PK11195 positron emission tomographic imaging in Alzheimer disease. Archives of neurology. https://doi.org/10.1001/archneurol.2008.511

Vancouver

Wiley CA, Lopresti BJ, Venneti S, Price J, Klunk WE, DeKosky ST, et al. Carbon 11-labeled Pittsburgh Compound B and carbon 11-labeled (R)-PK11195 positron emission tomographic imaging in Alzheimer disease. Archives of neurology. 2009. doi:10.1001/archneurol.2008.511. PMID: 19139300.

BibTeX

@article{wiley2009-19139300,
  author  = {Wiley, C. A. and Lopresti, B. J. and Venneti, S. and Price, J. and Klunk, W. E. and DeKosky, S. T. and Mathis, C. A.},
  title   = {{Carbon 11-labeled Pittsburgh Compound B and carbon 11-labeled (R)-PK11195 positron emission tomographic imaging in Alzheimer disease}},
  journal = {Archives of neurology},
  year    = {2009},
  doi     = {10.1001/archneurol.2008.511},
  pmid    = {19139300},
  url     = {https://doi.org/10.1001/archneurol.2008.511}
}

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