2013
DOI: 10.1371/journal.pone.0068159
|View full text |Cite
|
Sign up to set email alerts
|

Anti-Aggregating Effect of the Naturally Occurring Dipeptide Carnosine on Aβ1-42 Fibril Formation

Abstract: Carnosine is an endogenous dipeptide abundant in the central nervous system, where by acting as intracellular pH buffering molecule, Zn/Cu ion chelator, antioxidant and anti-crosslinking agent, it exerts a well-recognized multi-protective homeostatic function for neuronal and non-neuronal cells. Carnosine seems to counteract proteotoxicity and protein accumulation in neurodegenerative conditions, such as Alzheimer’s Disease (AD). However, its direct impact on the dynamics of AD-related fibril formation remains… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

2
54
0
1

Year Published

2014
2014
2024
2024

Publication Types

Select...
9
1

Relationship

0
10

Authors

Journals

citations
Cited by 66 publications
(57 citation statements)
references
References 76 publications
2
54
0
1
Order By: Relevance
“…Our expanding knowledge of tauopathy in AD brains, including intracellular tangles and threads of aggregated pTau, has grown to encompass a diversity of extracellular soluble and insoluble assemblies, which may induce seed-like self-propagation into synaptically dense regions [11, 33, 66, 77, 84, 94, 182]. Currently, the detection of plaques and NFTs by histological brain examination at autopsy provides the most definitive diagnosis of AD [4, 55, 76, 81, 88, 95, 166]. Although plaque burden may plateau at a presymptomatic stage of the disease, obscuring its relationship with disease progression, it is postulated that the early assemblies of misfolded Aβ also elicit chronic, low-grade neuroinflammation that correlates with cognitive decline [27, 131, 153, 169, 186].…”
Section: Introductionmentioning
confidence: 99%
“…Our expanding knowledge of tauopathy in AD brains, including intracellular tangles and threads of aggregated pTau, has grown to encompass a diversity of extracellular soluble and insoluble assemblies, which may induce seed-like self-propagation into synaptically dense regions [11, 33, 66, 77, 84, 94, 182]. Currently, the detection of plaques and NFTs by histological brain examination at autopsy provides the most definitive diagnosis of AD [4, 55, 76, 81, 88, 95, 166]. Although plaque burden may plateau at a presymptomatic stage of the disease, obscuring its relationship with disease progression, it is postulated that the early assemblies of misfolded Aβ also elicit chronic, low-grade neuroinflammation that correlates with cognitive decline [27, 131, 153, 169, 186].…”
Section: Introductionmentioning
confidence: 99%
“…Recently, a study was performed investigating the effects of carnosine on the formation of peptide fragment Aβ1-42 aggregates. Atomic force microscopy and thioflavin T assays showed an inhibition of Aβ1-42 fibrillogenesis in vitro and differences in the aggregation state of Aβ1-42 small prefibrillar structures in the presence of carnosine [83], suggesting that carnosine may be effective against the Aβ aggregation in AD brain.…”
Section: Alzheimer's Disease (Ad)mentioning
confidence: 93%
“…Działanie przeciwstarzeniowe karnozyny i anseryny może z kolei wynikać z ich właściwości prowadzących do spowolnienia procesu skracania się telomerów w chromosomach [53,54]. Karnozyna ponadto zwiększa wrażliwość insulinową [55], poprawia stan zdrowia pacjentów w przypadku choroby Alzheimera [56], Parkinsona [57], miażdżycy [58], chorobach nerek spowodowanych cukrzycą [59] oraz przyspiesza gojenie ran [60].…”
Section: Karnozyna I Anserynaunclassified