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Zonneveld HI, Goos JD, Wattjes MP, Prins ND, Scheltens P, van der Flier WM, Kuijer JP, Muller M, Barkhof F. Prevalence of cortical superficial siderosis in a memory clinic population. Neurology. 2014 Feb 25;82(8):698-704. Epub 2014 Jan 29 PubMed.
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Mayo Clinic
The study by Kantarci et al. investigating the focal hemosiderin deposits in the form of microhemorrhages and superficial siderosis in the ADNI cohort (Kantarci et al., 2013), reported that a majority of individuals with superficial siderosis also have microhemorrhages, in agreement with the current study. The prevalence of superficial siderosis in patents with AD was lower in the ADNI cohort (1/40, or 2.5 percent) compared with the prevalence of superficial siderosis in the current study. There are differences in the memory clinic cohort reported in the current study and ADNI that are important to consider when comparing the two. ADNI is designed to represent cohorts typically recruited to clinical trials for the treatment and prevention of AD. Thus, ADNI does not include individuals with significant cerebrovascular disease. In contrast, the memory clinic cohort reported in the current study did not exclude AD patients with cerebrovascular disease, which may have increased the number of cerebral amyloid angiopathy cases and associated superficial siderosis in this cohort. Superficial siderosis is associated with cerebral amyloid angiopathy and its prevalence may be lower in AD cohorts who are selected for clinical trials.
References:
Kantarci K, Gunter JL, Tosakulwong N, Weigand SD, Senjem MS, Petersen RC, Aisen PS, Jagust WJ, Weiner MW, Jack CR, . Focal hemosiderin deposits and β-amyloid load in the ADNI cohort. Alzheimers Dement. 2013 Oct;9(5 Suppl):S116-23. PubMed.
Erasmus MC University Medical Center
This present report by Zonneveld et al. is interesting as it shows that in a large memory clinic population, there is 1) a link between AD and superficial siderosis (SS), 2) a link between microbleeds and SS in AD patients, and 3) a higher prevalence of SS in MCI patients versus controls. Together, combined with previous reports of SS in cerebral amyloid angiopathy (CAA), these findings point toward SS being a sign of amyloid angiopathy in AD, and possibly also in MCI. I have only one minor point of critique, which is regarding the location of SS described by the authors. They found SS to occur more often in the frontal and parietal lobe compared with the occipital lobe. Yet taking into account the much larger volume of both the frontal lobe and parietal lobe compared to that of the occipital lobe, proportionally the prevalence of SS in the occipital lobe was very high in my opinion. This is interesting as the distribution of CAA pathology in CAA patients is known to be preferentially occipital—again, these findings are thus in line with SS reflecting amyloid angiopathy in this population.
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