scholarly journals Absence of ALOX5 gene prevents stress-induced memory deficits, synaptic dysfunction and tauopathy in a mouse model of Alzheimer's disease

2014 ◽  
Vol 23 (25) ◽  
pp. 6894-6902 ◽  
Author(s):  
Y. B. Joshi ◽  
P. F. Giannopoulos ◽  
J. Chu ◽  
M. Sperow ◽  
L. G. Kirby ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Memory Deficits ◽  
Synaptic Dysfunction ◽  
Model Of Alzheimer’S Disease

scholarly journals Impaired AMPA signaling and cytoskeletal alterations induce early synaptic dysfunction in a mouse model of Alzheimer's disease

Aging Cell ◽  
2018 ◽  
Vol 17 (4) ◽  
pp. e12791 ◽  
Author(s):  
David Baglietto-Vargas ◽  
Gilberto Aleph Prieto ◽  
Agenor Limon ◽  
Stefania Forner ◽  
Carlos J. Rodriguez-Ortiz ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Synaptic Dysfunction ◽  
Model Of Alzheimer’S Disease

scholarly journals Chiral gold nanoparticles enantioselectively rescue memory deficits in a mouse model of Alzheimer’s disease

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Ke Hou ◽  
Jing Zhao ◽  
Hui Wang ◽  
Bin Li ◽  
Kexin Li ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Gold Nanoparticles ◽  
Mouse Model ◽  
Chiral Recognition ◽  
Memory Deficits ◽  
Aβ Peptides ◽  
Promising Strategy ◽  
Model Of Alzheimer’S Disease ◽  
Behavioral Impairments

Abstract Preventing aggregation of amyloid beta (Aβ) peptides is a promising strategy for the treatment of Alzheimer’s disease (AD), and gold nanoparticles have previously been explored as a potential anti-Aβ therapeutics. Here we design and prepare 3.3 nm L- and D-glutathione stabilized gold nanoparticles (denoted as L3.3 and D3.3, respectively). Both chiral nanoparticles are able to inhibit aggregation of Aβ42 and cross the blood-brain barrier (BBB) following intravenous administration without noticeable toxicity. D3.3 possesses a larger binding affinity to Aβ42 and higher brain biodistribution compared with its enantiomer L3.3, giving rise to stronger inhibition of Aβ42 fibrillation and better rescue of behavioral impairments in AD model mice. This conjugation of a small nanoparticle with chiral recognition moiety provides a potential therapeutic approach for AD.

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