The existence of two groups of AD patients with different plasmin levels
suggests that disease-associated features such as inflammation or cell
death are not responsible for plasmin paucity. This view is reinforced
by the fact that the amount of amyloid plaques and tau filament
aggregation are similar for all AD samples (see supplementary material and Table 1).
Furthermore, variables such as age, sex, post-mortem brain sampling
delay, hippocampal area analysed, degree of dementia or cause of death
could also not be correlated to the alteration observed. On the other
hand, we observed that all individuals with normal plasmin levels, AD
and non-AD, carried either the E3/E3 or E3/E2 alleles of the
apolipoprotein E (ApoE), whereas all individuals with low plasmin
content carried at least one ApoE4 allele, a known risk factor for AD (Corder et al., 1993).
Although these data point to the existence of a link between AD ApoE4
and low plasmin, it is beyond the scope of this work to determine if
ApoE4 is a primary cause of this defect. Our goal remained to elucidate
what cellular requirements might have failed in this group of patients.