Peptides homologous to the amyloid protein of Alzheimer's disease containing a glutamine for glutamic acid substitution have accelerated amyloid fibril formation

1991 ◽  
Vol 179 (3) ◽  
pp. 1247-1254 ◽  
Author(s):  
Thomas Wisniewski ◽  
Jorge Ghiso ◽  
Blas Frangione
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Glutamic Acid ◽  
Amyloid Fibril ◽  
Fibril Formation ◽  
Amyloid Protein ◽  
Amyloid Fibril Formation

scholarly journals Spearmint Extract Containing Rosmarinic Acid Suppresses Amyloid Fibril Formation of Proteins Associated with Dementia

Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3480
Author(s):  
Kenjirou Ogawa ◽  
Ayumi Ishii ◽  
Aimi Shindo ◽  
Kunihiro Hongo ◽  
Tomohiro Mizobata ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Rosmarinic Acid ◽  
Lewy Body ◽  
Amyloid Fibrils ◽  
Amyloid Fibril ◽  
Lewy Body Dementia ◽  
Fibril Formation ◽  
Tau Proteins ◽  
Amyloid Fibril Formation

Neurological dementias such as Alzheimer’s disease and Lewy body dementia are thought to be caused in part by the formation and deposition of characteristic insoluble fibrils of polypeptides such as amyloid beta (Aβ), Tau, and/or α-synuclein (αSyn). In this context, it is critical to suppress and remove such aggregates in order to prevent and/or delay the progression of dementia in these ailments. In this report, we investigated the effects of spearmint extract (SME) and rosmarinic acid (RA; the major component of SME) on the amyloid fibril formation reactions of αSyn, Aβ, and Tau proteins in vitro. SME or RA was added to soluble samples of each protein and the formation of fibrils was monitored by thioflavin T (ThioT) binding assays and transmission electron microscopy (TEM). We also evaluated whether preformed amyloid fibrils could be dissolved by the addition of RA. Our results reveal for the first time that SME and RA both suppress amyloid fibril formation, and that RA could disassemble preformed fibrils of αSyn, Aβ, and Tau into non-toxic species. Our results suggest that SME and RA may potentially suppress amyloid fibrils implicated in the progression of Alzheimer’s disease and Lewy body dementia in vivo, as well.

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