Melatonin ameliorates amyloid beta-induced memory deficits, tau hyperphosphorylation and neurodegeneration via PI3/Akt/GSk3β pathway in the mouse hippocampus

2015 ◽  
Vol 59 (1) ◽  
pp. 47-59 ◽  
Author(s):  
Tahir Ali ◽  
Myeong Ok Kim
Keyword(s):  
Amyloid Beta ◽  
Memory Deficits ◽  
Tau Hyperphosphorylation ◽  
Mouse Hippocampus

Autophagy Enhancer Carbamazepine Alleviates Memory Deficits and Cerebral Amyloid-β Pathology in a Mouse Model of Alzheimer's Disease

2013 ◽  
Vol 10 (4) ◽  
pp. 433-441 ◽  
Author(s):  
Lixi Li ◽  
Sufang Zhang ◽  
Xin Zhang ◽  
Ting Li ◽  
Yu Tang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Amyloid Beta ◽  
Memory Deficits ◽  
Cerebral Amyloid

P2-488: Tudca, a bile acid, attenuates amyloid beta deposition and rescues memory deficits in app/ps1 mice

2011 ◽  
Vol 7 ◽  
pp. S468-S469
Author(s):  
Ana Nunes ◽  
Maria Fonseca ◽  
Ricardo Viana ◽  
Adrian Lo ◽  
Bart De Strooper ◽  
...  
Keyword(s):  
Bile Acid ◽  
Amyloid Beta ◽  
Memory Deficits

Berberine Alleviates Amyloid-Beta Pathology in the Brain of APP/PS1 Transgenic Mice via Inhibiting β/γ-Secretases Activity and Enhancing α-Secretases

2018 ◽  
Vol 15 (11) ◽  
pp. 1045-1052 ◽  
Author(s):  
Zhiyou Cai ◽  
Chuanling Wang ◽  
Wenbo He ◽  
Yi Chen
Keyword(s):  
Western Blotting ◽  
Amyloid Beta ◽  
Water Maze ◽  
Senile Plaque ◽  
Memory Deficits ◽  
Brain Diseases ◽  
Enzyme Linked Immunosorbent Assay ◽  
Neuroprotective Effects ◽  
Improved Learning ◽  
The Brain

Background: Berberine (BBR) has neuroprotective effects on many brain diseases, including Alzheimer’s disease (AD). Amyloid -beta (Aβ) senile plaque is the most classical pathological hallmarks of AD. Aβ produces from a sequential cleavage by β-secretase (beta-site amyloid precursor protein cleaving enzyme 1, BACE1) and γ -secretase. The aim of our work was to investigate whether the neuroprotective effects of BBR on AD is related to inhibiting Aβ pathology. Method: The cognitive function of mice was assessed by the Morris water maze (MWM) test. The Aβ levels were determined by enzyme linked immunosorbent assay; the expression of APP, sAPPα, ADAM10 and ADAM17, sAPPβ and BACE1 was detected by Western blotting; and the activity of γ -secretase complex (NCT, PS1, Aph-1α and Pen-2) was determined by Western blotting and immunohistochemistry. Results: BBR improved learning and memory deficits of APP/PS1 mice. BBR decreased Aβ levels in the hippocampus of APP/PS1 mice. BACE1 and sAPP -β levels in the BBR-treated groups were significantly reduced in the hippocampus of AD mice. BBR markedly decreased the expression of PS1, Aph-1α and Pen-2, but had no effect on NCT. The levels of sAPPα, ADAM10 and ADAM17 in the hippocampus of BBR-treated mice significantly increased, compared with the control ones (P<0.05). Conclusion: BBR inhibits the activity of β/γ-secretases, enhances α-secretases, and lowers the Aβ level in the hippocampus of AD mice, and improves Alzheimer’s-like cognitive impairment.

scholarly journals Arctigenin Attenuates Learning and Memory Deficits through PI3k/Akt/GSK-3β Pathway Reducing Tau Hyperphosphorylation in Aβ-Induced AD Mice

Planta Medica ◽  
2016 ◽  
Vol 83 (01/02) ◽  
pp. 51-56 ◽  
Author(s):  
Yue Qi ◽  
De-Qiang Dou ◽  
Hong Jiang ◽  
Bing-Bing Zhang ◽  
Wen-Yan Qin ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Memory Deficits ◽  
Tau Hyperphosphorylation ◽  
Learning And Memory Deficits ◽  
Gsk 3Β

scholarly journals Indirubin-3′-monoxime suppresses amyloid-beta-induced apoptosis by inhibiting tau hyperphosphorylation

2016 ◽  
Vol 11 (6) ◽  
pp. 0 ◽  
Author(s):  
Shu-gang Zhang ◽  
Xiao-shan Wang ◽  
Ying-dong Zhang ◽  
Qing Di ◽  
Jing-ping Shi ◽  
...  
Keyword(s):  
Amyloid Beta ◽  
Tau Hyperphosphorylation ◽  
Induced Apoptosis

scholarly journals Differential Inhibition of E-S Potentiation and Long-term Potentiation by Cell-derived and Arctic Amyloid Beta

2019 ◽  
Author(s):  
Adrienne L. Orr ◽  
Jason K. Clark ◽  
Daniel V. Madison
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Beta ◽  
Hippocampal Slices ◽  
Memory Deficits ◽  
Long Term Potentiation ◽  
Amyloid Beta Peptide ◽  
Term Potentiation ◽  
Beta Peptide

AbstractSoluble oligomers of amyloid-beta peptide (Abeta) have been implicated in the onset of memory deficits in Alzheimer’s disease, perhaps due to their reported ability to impair long-term potentiation (LTP) of synaptic strength. We previously showed the effect of Abeta on LTP depends on the strength of LTP induction. Furthermore, Abeta affects EPSP-Spike (E-S) potentiation more robustly than LTP, suggesting that E-S potentiation may be equally important to learning and memory in the context of Alzheimer’s disease. Here we extend our findings to two additional forms of Abeta that form higher concentrations of soluble Abeta oligomers and show that they also affect E-S potentiation at induction strengths where there is no effect on LTP in hippocampal slices.

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