Acta Neuropathologica: Coarse-grained plaques: a different type of A-beta plaque in early-haired Alzheimer's disease.

Amyloid beta (A beta) plaques and high phosphate tau (pTau) tangles are the main pathological characteristics of Alzheimer's disease (AD).
A beta plaque originated from the accumulation and aggregation of A-beta peptides and was formed by the continuous lysing of amyloid prebiotic proteins by beta-secretase and gamma-secretase.
the length of A-beta peptides may vary from 36 to 43 amino acids, with A-beta 40 and A-beta 42 being the most common forms in AD, depending on the lysate point of the gamma-secretase.
longer A-beta-42 is more likely to accumulate, mainly in the brain's essential plaques, while the shorter A-beta-40 is secreted by higher-level cells and is the main A-beta subtype deposited in the cerebrovascular system, known as cerebral amyloid vascular disease (CAA).
, we observed an atypical A-beta deposit, called coarse plaque.
study, we assessed the relationship between plaques and clinical diseases and conducted in-depth immunological and morphological identification.
coarse particle plaque is a relatively large sediment characterized by multi-core and A-beta-free pores, which are prominent in the new cortical.
a semi-quantitative score of plaques back in the preletains of 74 patients with a positive A(n-74), including non-dementia patients (n-15), early hair (EO) AD (n-38), and late-haired (LO) AD (n-21).
coarse particle plaques have only been observed in patients with clinical dementia and are more common in EOAD than in LOAD.
the plaque was associated with pure APOE 4 status and cerebral amyloid vascular disease (CAA).
by studying the neuroinflamed components (pTau, APP, PrPC), A-beta subtypes (A beta 40, A beta 42, A beta N3pE, pSer8A beta), its neuro-inflammatory components (C4b, CD68, MHC-II, GFAP) and their vascular properties (layer adhesion protein, IV collagen, norrin).
the plaques with classic core patches, cotton patches, and CAA.
similar to CAA, but unlike classical core plaques, coarse plaques consist mainly of A-beta 40.
addition, coarse particle plaques are significantly associated with intense neuroprotein inflammation and vascular (capillary) pathology.
cofocus laser scanning microscope (CLSM) and 3D analysis showed that most coarse plaques have a special A-beta 40 shell structure and are directly related to blood vessels.
based on its morphological and bio-chemical characteristics, we consider coarse particle plaques to be a dispersion-type A-beta plaque associated with EOAD.
of coarse particle plaques from other A-beta deposits may be due to differences in A-beta processing and aggregation, neuro-inflammatory responses, and vascular removal.
in the search for treatment based on disease mechanisms, it may be important to isolate AD subgroup-specific A-beta deposition.
methods: continuous chemical biopsy of sumutin and Irau (H&E), Congolese red, A beta (aa 8-17), A beta 40, A beta 42, A beta N3pE, pSer8A beta, APP, PrPC, pTau, C4b, MHC-II, GFAP, norrin, layer adhesive protein, IV collagen, and lipoprotein E.
the slice (5min) with sumu essence, then soak the slice with erythew (3min) for H.E.
Congo Red tissue chemistry is incubated at room temperature with a saturated sodium chloride solution (3% sodium chloride in 80% ethanol and 1% 1 M NaOH) and then incubated at room temperature with a saturated Congolese red solution (0.25% Congolese red dissolved in 80% ethanol and 1% 1 M NaOH), both at room temperature for 20 minutes.
endogenous peroxidase with 0.3% H2O2 in phosphate buffer (PBS; ph7.4) or methanol annihilation.
followed by appropriate antigen recovery and primary antibody culture.
then, the slices are cultured with secondary antibodies, then colored with 3,3'-daminophenyl phenylamine (DAB) (Angelendaco) and re-dyed with sumu.
between the two steps, rinse the slices with PBS.
, in this study, we described and defined a new type of A-beta deposition called coarse plaque.
we provide morphological and biochemical definitions of coarse plaques that support this deposition is unique and has specific clinical and pathogenic links.
related disease mechanisms such as neuroinstation and vascular properties, as well as the structure and biobiological composition of A-beta may be the cause of differences in A-beta deposition patterns.
in the near future, isolating specific A-beta deposits between AD sub-groups may be important in finding treatments based on disease mechanisms.
Boon, B.D.C., Bulk, M., Jonker, A.J. et al. The coarse-grained plaque: a divergent A beta plaque-type in early-onset Alzheimer's disease. Acta Neuropathol (2020) MedSci Original Source: MedSci Original Copyright Notice: All text, images and audio and video materials on this website that indicate "Source: Mets Medicine" or "Source: MedSci Original" are owned by Mets Medical and are not licensed and may not be reproduced by any media, website or individual, and shall be reproduced with the words "Source: Mets Medicine".
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