Apoptosis, rather than neurogenesis, induces significant hippocampal‐dependent learning and memory impairment in chronic low Cd 2+ exposure

2022 ◽  
Author(s):  
Tianpeng Li ◽  
Shuyan Dong ◽  
Jiancheng He ◽  
Jing Yang ◽  
Weiyun Li ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Memory Impairment ◽  
Dependent Learning

Beta amyloid-induced time-dependent learning and memory impairment: involvement of HPA axis dysfunction

2020 ◽  
Vol 35 (8) ◽  
pp. 1385-1394
Author(s):  
Jinpeng Lv ◽  
Ling Chen ◽  
Naping Zhu ◽  
Yindi Sun ◽  
Jianchun Pan ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Hpa Axis ◽  
Memory Impairment ◽  
Beta Amyloid ◽  
Time Dependent ◽  
Dependent Learning

scholarly journals Clock/Sleep-Dependent Learning and Memory in Male 3xTg-AD Mice at Advanced Disease Stages and Extrinsic Effects of Huprine X and the Novel Multitarget Agent AVCRI104P3

2021 ◽  
Vol 11 (4) ◽  
pp. 426
Author(s):  
Lydia Giménez-Llort ◽  
Mikel Santana-Santana ◽  
Míriam Ratia ◽  
Belén Pérez ◽  
Pelayo Camps ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Advanced Disease ◽  
Active Phase ◽  
Task Demands ◽  
The Novel ◽  
Training Time ◽  
Drug Effectiveness ◽  
Dependent Learning ◽  
Disease Stages

A new hypothesis highlights sleep-dependent learning/memory consolidation and regards the sleep-wake cycle as a modulator of β-amyloid and tau Alzheimer’s disease (AD) pathologies. Sundowning behavior is a common neuropsychiatric symptom (NPS) associated with dementia. Sleep fragmentation resulting from disturbances in sleep and circadian rhythms in AD may have important consequences on memory processes and exacerbate the other AD-NPS. The present work studied the effect of training time schedules on 12-month-old male 3xTg-AD mice modeling advanced disease stages. Their performance in two paradigms of the Morris water maze for spatial-reference and visual-perceptual learning and memory were found impaired at midday, after 4 h of non-active phase. In contrast, early-morning trained littermates, slowing down from their active phase, exhibited better performance and used goal-directed strategies and non-search navigation described for normal aging. The novel multitarget anticholinesterasic compound AVCRI104P3 (0.6 µmol·kg−1, 21 days i.p.) exerted stronger cognitive benefits than its in vitro equipotent dose of AChEI huprine X (0.12 μmol·kg−1, 21 days i.p.). Both compounds showed streamlined drug effectiveness, independently of the schedule. Their effects on anxiety-like behaviors were moderate. The results open a question of how time schedules modulate the capacity to respond to task demands and to assess/elucidate new drug effectiveness.

scholarly journals Ferroptosis contributes to isoflurane-induced neurotoxicity and learning and memory impairment

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Pengfei Liu ◽  
Jing Yuan ◽  
Yetong Feng ◽  
Xin Chen ◽  
Guangsuo Wang ◽  
...  
Keyword(s):  
Cell Death ◽  
Learning And Memory ◽  
Memory Impairment ◽  
Close Association ◽  
Dimethyl Fumarate ◽  
Dependent Manner ◽  
Transport Chain ◽  
The Relationship

AbstractFerroptosis is a novel type of programmed cell death, which is different from apoptosis and autophagic cell death. Recently, ferroptosis has been indicated to contribute to the in vitro neurotoxicity induced by isoflurane, which is one of the most common anesthetics in clinic. However, the in vivo position of ferroptosis in isoflurane-induced neurotoxicity as well as learning and memory impairment remains unclear. In this study, we mainly explored the relationship between ferroptosis and isoflurane-induced learning and memory, as well as the therapeutic methods in mouse model. Our results indicated that isoflurane induced the ferroptosis in a dose-dependent and time-dependent manner in hippocampus, the organ related with learning and memory ability. In addition, the activity of cytochrome c oxidase/Complex IV in mitochondrial electron transport chain (ETC) was increased by isoflurane, which might further contributed to cysteine deprivation-induced ferroptosis caused by isoflurane exposure. More importantly, isoflurane-induced ferroptosis could be rescued by both ferroptosis inhibitor (ferrostatin-1) and mitochondria activator (dimethyl fumarate), which also showed effective therapeutic action against isoflurane-induced learning and memory impairment. Taken together, our data indicate the close association among ferroptosis, mitochondria and isoflurane, and provide a novel insight into the therapy mode against isoflurane-induced learning and memory impairment.

Effects of repeated administration of (−)-nicotine on AF64A-induced learning and memory impairment in rats

2002 ◽  
Vol 109 (3) ◽  
pp. 361-375 ◽  
Author(s):  
M. Hiramatsu ◽  
T. Yamatsu ◽  
T. Kameyama ◽  
T. Nabeshima
Keyword(s):  
Learning And Memory ◽  
Memory Impairment ◽  
Repeated Administration

scholarly journals Amelioration of Scopolamine-Induced Learning and Memory Impairment byα-Pinene in C57BL/6 Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Gil-Yong Lee ◽  
Chan Lee ◽  
Gyu Hwan Park ◽  
Jung-Hee Jang
Keyword(s):  
Learning And Memory ◽  
Memory Impairment ◽  
Manganese Superoxide Dismutase ◽  
Molecular Mechanisms ◽  
Neuroprotective Effect ◽  
Memory Loss ◽  
Cholinergic Neurons ◽  
Morris Water Maze Test ◽  
Heme Oxygenase 1 ◽  
Related Factor

Increasing evidence suggests that neurodegenerative disorders such as Alzheimer’s disease (AD) are mediated via disruption of cholinergic neurons and enhanced oxidative stress. Therefore, attention has been focused on searching for antioxidant phytochemicals for the prevention and/or treatment of AD through their ability to fortify cholinergic function and antioxidant defense capacity. In this study, we have investigated the neuroprotective effect ofα-pinene (APN) against learning and memory impairment induced by scopolamine (SCO, 1 mg/kg, i.p.), a muscarinic receptor antagonist in C57BL/6 mice. Administration of APN (10 mg/kg, i.p.) significantly improved SCO-induced cognitive dysfunction as assessed by Y-maze and passive avoidance tests. In Morris water-maze test, APN effectively shortened the mean escape latency to find the hidden platform during training days. To further elucidate the molecular mechanisms underlying the neuroprotective effect of APN, the expression of proteins involved in the acetylcholine metabolism and antioxidant system was examined. Particularly, APN treatment increased mRNA expression of choline acetyltransferase in the cortex and protein levels of antioxidant enzymes such as heme oxygenase-1 and manganese superoxide dismutase in the hippocampus via activation of NF-E2-related factor 2. These findings suggest the possible neuroprotective potentials of APN for the management of dementia with learning and memory loss.

Pharmacological profile of OPC-14523 (2): Effects on learning and memory impairment

1996 ◽  
Vol 6 ◽  
pp. 189
Author(s):  
M. Nakai ◽  
K. Tottori ◽  
T. Kikuchi ◽  
Y. Uwahodo ◽  
T. Miwa ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Memory Impairment ◽  
Pharmacological Profile
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