In contrast, PrPSc accumulation was noted in the cerebellum of both published E200K-129V cases; the E200K-129V V) patient with predominant plaque-like PrP deposits [ 29] and the E200K-129V(M) patient with focal PrPSc deposits with a perpendicular orientation to the pial surface in the cerebellar molecular layer [ 17].
These studies indicate that local anti-inflammatory effects of Ccr2 and Ndst1 deficiency inherent in the donor transplant, carried over to the recipient mouse and have predominant effects on plaque growth in the mouse aortic allograft transplant model.
Moreover, LMP2 expression was predominant in MS plaques (Fig. 2A) compared to pre-plaque white matter and cortex while in the same CNS area of control only luminal endothelial cells were stained (Fig. 2B).
Cases with predominant cotton-wool plaques (PSEN1 PSEN1, Pshowed286P) showed fewer APP-immunoreactive dystrophic neurites than ADAD cases with neuritic plaques (Fig. 4).
M2 macrophages were infiltrated in early lesions of ApoE−/− mice, while M1 macrophages were predominant in advanced plaques of aged animals [ 15].
The major source for MMPs is also immigrated monocytes/macrophages and vascular smooth muscle cells [17], and MMP-9 seems to be one of the predominant MMPs within the vulnerable plaque, where it promotes plaque progression and destabilization [18], [19].
Goate and Valdivieso suspect that 491A might contribute to the formation of protein plaques, a hallmark of Alzheimer's disease, by stepping up production of apoE, the predominant protein in the plaques.
The same observation is made in inherited prion disease with the predominant formation of cerebellar plaques, such as P102L GSS, where tau is associated with, but not limited to, plaques.
The plaque-predominant type with abundant amyloid plaques, with no or very little neuritic pathology restricted to the hippocampus and with abnormal phosphorylated tau in neocortical pyramidal cells, but lacking overt tangle formation, accounts for 3.5 to 8% of demented subjects over age 85 years [ 6].
Aβ42 makes up only 10% of the total Aβ, but is the more predominant toxic species found in plaques due to its enhanced hydrophobicity, aggregation and fibrillization potential.
