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53/100

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Genetics

Topic: Amyloid, tau and blood-test diagnosis

Plain-language summary

Background A subset of patients with cerebral amyloid angiopathy (CAA) present with cognitive symptoms, seizures, headaches, T2-hyperintense MRI lesions, and neuropathologic evidence of CAA-associated vascular inflammation. Objective To analyze the risk factors, diagnostic characteristics, and long-term course of this disorder. Methods We assessed 14 consecutive patients with pathologically diagnosed CAA-related inflammation, 12 with available neuroimaging and follow-up data. Patients were evaluated for MRI appearance, APOE genotype, and clinical course over a 46.8 +/- 29.1-month follow-up. Results Baseline MRI scans were characterized by asymmetric T2-hyperintense lesions extending to the subcortical white matter and occasionally the overlying gray matter, with signal properties suggesting vasogenic edema. Subjects could be divided into three groups based on response to immunosuppressive treatment: monophasic improvement (7/12), initial improvement followed by symptomatic relapse (3/12), and no evident response to treatment (2/12). The volume of MRI hyperintensities correlated with the severity of clinical symptoms. One patient experienced symptomatic intracerebral hemorrhage within a region of recurrent MRI hyperintensity. The APOE epsilon4/epsilon4 genotype was strongly associated with CAA-related inflammation, present in 76.9% (10/13) of subjects vs 5.1% (2/39) with symptomatic but noninflammatory CAA (p Conclusion Cerebral amyloid angiopathy-related inflammation represents a clinically, pathologically, radiographically, and genetically distinct disease subtype with implications for clinical practice and ongoing immunotherapeutic approaches to Alzheimer disease.

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APA 7th

Kinnecom, C., Lev, M. H., Wendell, L., Smith, E. E., Rosand, J., Frosch, M. P., et al. (2007). Course of cerebral amyloid angiopathy-related inflammation. Neurology. https://doi.org/10.1212/01.wnl.0000260066.98681.2e

Vancouver

Kinnecom C, Lev MH, Wendell L, Smith EE, Rosand J, Frosch MP, et al. Course of cerebral amyloid angiopathy-related inflammation. Neurology. 2007. doi:10.1212/01.wnl.0000260066.98681.2e. PMID: 17452586.

BibTeX

@article{kinnecom2007-17452586,
  author  = {Kinnecom, C. and Lev, M. H. and Wendell, L. and Smith, E. E. and Rosand, J. and Frosch, M. P. and Greenberg, S. M.},
  title   = {{Course of cerebral amyloid angiopathy-related inflammation}},
  journal = {Neurology},
  year    = {2007},
  doi     = {10.1212/01.wnl.0000260066.98681.2e},
  pmid    = {17452586},
  url     = {https://doi.org/10.1212/01.wnl.0000260066.98681.2e}
}

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.

How to read this study

Design: our record does not state a study design, so check the methods section of the original before weighing the result.
Size: the record gives no participant count. Look for one in the original before trusting a pattern.
Effect: the record reports “76.9%; 5.1%”. A statistically significant result can still be small in daily life.

What the evidence grade means here

This page is graded low. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Low means the abstract matched neither pattern. It is the default label, and it does not mean the work is poor; many sound lab and imaging papers land here. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

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Key findings

Results Baseline MRI scans were characterized by asymmetric T2-hyperintense lesions extending to the subcortical white matter and occasionally the overlying gray matter, with signal properties suggesting vasogenic edema.
The APOE epsilon4/epsilon4 genotype was strongly associated with CAA-related inflammation, present in 76.9% (10/13) of subjects vs 5.1% (2/39) with symptomatic but noninflammatory CAA (p < 0.0001).

Why it matters

This study describes the course of cerebral amyloid angiopathy-related inflammation, including MRI findings, response to immunosuppressive treatment, and a strong link to the APOE epsilon 4/epsilon 4 genotype. It concerns this specific inflammatory condition rather than Alzheimer disease treatment, cure, or prevention.

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Study details

Effect size76.9%; 5.1%
Evidence strengthLow

How this study scored 53/100

Published in a leading specialty journal. Scored zero for study design, sample size, studied in people and randomized / blinded because the record does not state it.

Component	Points	Why
Journal tier	9 / 10	Tier 2 — leading specialty journal (Neurology)
Journal's citation record	4 / 4	Neurology: journal h-index 525 (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	2007 — 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	2 / 3	Effect reported as a number, without an interval or test
Studied in people	0 / 3	Not stated whether this was studied in people — scores zero (not stated in the record — scored 0)
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	6 / 7	Cited 334 times (OpenAlex, 2026-10-10)
Citations per year	3 / 5	15.9 citations a year over 21 year(s) since 2007
Impact for its field and year	4 / 6	Cited 8.8× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	3 / 6	Cited by 19 other studies in this library
Still being cited	2 / 4	Cited 39 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	4 / 4	Last-listed author Steven Mark Greenberg: h-index 144 (OpenAlex, whole career)
Institution's track record	2 / 3	Massachusetts General Hospital: institution h-index 2,057 (OpenAlex)
Multicenter collaboration	0 / 3	OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete)
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 17452586)
Free to read	0 / 2	Behind a paywall — scores zero
Total	53 / 100	—

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