Assembly of Aβ Amyloid Protofibrils:  An in Vitro Model for a Possible Early Event in Alzheimer's Disease†

Biochemistry ◽  
1999 ◽  
Vol 38 (28) ◽  
pp. 8972-8980 ◽  
Author(s):  
James D. Harper ◽  
Stanislaus S. Wong ◽  
Charles M. Lieber ◽  
Peter T. Lansbury
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
In Vitro Model ◽  
Early Event ◽  
Aβ Amyloid ◽  
Vitro Model

scholarly journals Comparative Effects of Alpha- and Gamma-Tocopherol on Mitochondrial Functions in Alzheimer’s Disease In Vitro Model

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Aslina Pahrudin Arrozi ◽  
Siti Nur Syazwani Shukri ◽  
Wan Zurinah Wan Ngah ◽  
Yasmin Anum Mohd Yusof ◽  
Mohd Hanafi Ahmad Damanhuri ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
In Vitro Model ◽  
Gamma Tocopherol ◽  
Mitochondrial Functions ◽  
Vitro Model

P1-124: Lithium Treatment Prevents Amyloid Toxicity and MIR-489 Down-Regulation in an Alzheimer’s Disease in Vitro MODEL

2016 ◽  
Vol 12 ◽  
pp. P451-P451
Author(s):  
Victor Junji Yamamoto ◽  
Vanessa de Jesus de Paula ◽  
Giancarlo de Mattos Cardillo ◽  
Orestes Vicente Forlenza ◽  
Wagner Farid Gattaz ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
In Vitro Model ◽  
Lithium Treatment ◽  
Down Regulation ◽  
Amyloid Toxicity ◽  
Vitro Model

scholarly journals The Moringin/α-CD Pretreatment Induces Neuroprotection in an In Vitro Model of Alzheimer’s Disease: A Transcriptomic Study

2021 ◽  
Vol 43 (1) ◽  
pp. 197-214
Author(s):  
Serena Silvestro ◽  
Luigi Chiricosta ◽  
Agnese Gugliandolo ◽  
Renato Iori ◽  
Patrick Rollin ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
In Vitro Model ◽  
Neurodegenerative Disorder ◽  
Senile Dementia ◽  
Neuroprotective Effects ◽  
Model Of Alzheimer’S Disease ◽  
Vitro Model ◽  
Ad Prevention

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and represents the most common form of senile dementia. Autophagy and mitophagy are cellular processes that play a key role in the aggregation of β-amyloid (Aβ) and tau phosphorylation. As a consequence, impairment of these processes leads to the progression of AD. Thus, interest is growing in the search for new natural compounds, such as Moringin (MOR), with neuroprotective, anti-amyloidogenic, antioxidative, and anti-inflammatory properties that could be used for AD prevention. However, MOR appears to be poorly soluble and stable in water. To increase its solubility MOR was conjugated with α-cyclodextrin (MOR/α-CD). In this work, it was evaluated if MOR/α-CD pretreatment was able to exert neuroprotective effects in an AD in vitro model through the evaluation of the transcriptional profile by next-generation sequencing (NGS). To induce the AD model, retinoic acid-differentiated SH-SY5Y cells were exposed to Aβ1-42. The MOR/α-CD pretreatment reduced the expression of the genes which encode proteins involved in senescence, autophagy, and mitophagy processes. Additionally, MOR/α-CD was able to induce neuronal remodeling modulating the axon guidance, principally downregulating the Slit/Robo signaling pathway. Noteworthy, MOR/α-CD, modulating these important pathways, may induce neuronal protection against Aβ1-42 toxicity as demonstrated also by the reduction of cleaved caspase 3. These data indicated that MOR/α-CD could attenuate the progression of the disease and promote neuronal repair.

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