Diffuse Plaques (DP) |
Lack a dense core usually large (50μm and more), moderate immunoreactive, amyloid bundles in the neuropil without degenerating neurites and accompanying microglia |
Both AD and non-AD older brains |
Generally do not induce a strong inflammatory response. Often found in cognitively normal aging brains. |
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Cored Plaques (CP) |
Characterized by a dense core of amyloid surrounded by a halo/corona of prematured fibrils. Typically stains intensely with amyloid-binding dyes. |
Typical for AD brains |
Strongly linked with cognitive decline and commonly observed in symptomatic AD cases. |
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Neuritic Plaques (NP) |
Include a dense core with surrounding corona, associated with neuritic processes, and with dystrophic neurites |
Non-demented elderly individuals, represent asymptomatic or preclinical AD (pre-AD) but also in fAD. |
Considered a hallmark of AD pathology and correlate with disease severity. Often surrounded by reactive glial cells. Distinguishable by MALDI MSI and PHF-1(IHC). |
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Fibrillar Plaques (FP) |
Dense-core plaques that are thioflavin-S and Congo red positive, indicating the presence of fibrils and Aβx-40 peptide along with higher AβxpE-42 |
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Associated with neuronal damage and are often surrounded by dystrophic neurites. |
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Coarse Grain Plaques (CG) |
Subtype of FP, characterized by dense amyloid deposition without corona and more abundant neuritic component |
Early onset AD and ApoE4 |
Show higher levels of Aβx-40 and less Aβx-42 compared to cored plaques. Linked to a higher degree of neuritic dystrophy. |
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Cotton Wool Plaques (CWP) |
Large, amorphous, and fluffy plaques without a compact amyloid core, found in some familial AD cases. |
Familial AD cases, presenilin-1 mutant cases of autosomal dominant AD |
Associated with specific genetic mutations, but not necessarily. Typically lack a fibrillar structure and do not bind thioflavin-S.. |
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