scholarly journals Dysregulated expression of monoacylglycerol lipase is a marker for anti-diabetic drug metformin-targeted therapy to correct impaired neurogenesis and spatial memory in Alzheimer's disease

Theranostics ◽  
2020 ◽  
Vol 10 (14) ◽  
pp. 6337-6360
Author(s):  
Charvi Syal ◽  
Jayasankar Kosaraju ◽  
Laura Hamilton ◽  
Anne Aumont ◽  
Alphonse Chu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Targeted Therapy ◽  
Spatial Memory ◽  
Monoacylglycerol Lipase ◽  
Impaired Neurogenesis

Intranasal administration of mitochondria improves spatial memory in olfactory bulbectomized mice

2021 ◽  
pp. 153537022110568
Author(s):  
Natalia V Bobkova ◽  
Daria Y Zhdanova ◽  
Natalia V Belosludtseva ◽  
Nikita V Penkov ◽  
Galina D Mironova
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Spatial Memory ◽  
Intranasal Administration ◽  
Brain Structures ◽  
Brain Regions ◽  
Dependent Manner ◽  
Behavioral Experiments ◽  
Hippocampal Cell Culture ◽  
The Brain

Here, we found that functionally active mitochondria isolated from the brain of NMRI donor mice and administrated intranasally to recipient mice penetrated the brain structures in a dose-dependent manner. The injected mitochondria labeled with the MitoTracker Red localized in different brain regions, including the neocortex and hippocampus, which are responsible for memory and affected by degeneration in patients with Alzheimer's disease. In behavioral experiments, intranasal microinjections of brain mitochondria of native NMRI mice improved spatial memory in the olfactory bulbectomized (OBX) mice with Alzheimer’s type degeneration. Control OBX mice demonstrated loss of spatial memory tested in the Morris water maze. Immunocytochemical analysis revealed that allogeneic mitochondria colocalized with the markers of astrocytes and neurons in hippocampal cell culture. The results suggest that a non-invasive route intranasal administration of mitochondria may be a promising approach to the treatment of neurodegenerative diseases characterized, like Alzheimer's disease, by mitochondrial dysfunction.

Ameliorative effect of sansoninto on sleep disturbance and spatial memory impairment in an Alzheimer's disease rat model

2017 ◽  
Vol 4 (1) ◽  
pp. 38-45 ◽  
Author(s):  
Hiroshi Moriyama ◽  
Takuya Watanabe ◽  
Kotaro Takasaki ◽  
Masaki Nagao ◽  
Kaori Kubota ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Spatial Memory ◽  
Sleep Disturbance ◽  
Rat Model ◽  
Memory Impairment ◽  
Ameliorative Effect

scholarly journals Regional differences in Alzheimer’s disease pathology confound behavioural rescue after amyloid-β attenuation

Brain ◽  
2019 ◽  
Vol 143 (1) ◽  
pp. 359-373 ◽  
Author(s):  
Christopher D Morrone ◽  
Paolo Bazzigaluppi ◽  
Tina L Beckett ◽  
Mary E Hill ◽  
Margaret M Koletar ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Trials ◽  
Cognitive Function ◽  
Spatial Memory ◽  
Regional Differences ◽  
Amyloid Β ◽  
Amyloid Β Peptide ◽  
Barnes Maze ◽  
Tau Pathology

Abstract Failure of Alzheimer’s disease clinical trials to improve or stabilize cognition has led to the need for a better understanding of the driving forces behind cognitive decline in the presence of active disease processes. To dissect contributions of individual pathologies to cognitive function, we used the TgF344-AD rat model, which recapitulates the salient hallmarks of Alzheimer’s disease pathology observed in patient populations (amyloid, tau inclusions, frank neuronal loss, and cognitive deficits). scyllo-Inositol treatment attenuated amyloid-β peptide in disease-bearing TgF344-AD rats, which rescued pattern separation in the novel object recognition task and executive function in the reversal learning phase of the Barnes maze. Interestingly, neither activities of daily living in the burrowing task nor spatial memory in the Barnes maze were rescued by attenuating amyloid-β peptide. To understand the pathological correlates leading to behavioural rescue, we examined the neuropathology and in vivo electrophysiological signature of the hippocampus. Amyloid-β peptide attenuation reduced hippocampal tau pathology and rescued adult hippocampal neurogenesis and neuronal function, via improvements in cross-frequency coupling between theta and gamma bands. To investigate mechanisms underlying the persistence of spatial memory deficits, we next examined neuropathology in the entorhinal cortex, a region whose input to the hippocampus is required for spatial memory. Reduction of amyloid-β peptide in the entorhinal cortex had no effect on entorhinal tau pathology or entorhinal-hippocampal neuronal network dysfunction, as measured by an impairment in hippocampal response to entorhinal stimulation. Thus, rescue or not of cognitive function is dependent on regional differences of amyloid-β, tau and neuronal network dysfunction, demonstrating the importance of staging disease in patients prior to enrolment in clinical trials. These results further emphasize the need for combination therapeutic approaches across disease progression.

IL12/23 p40 Inhibition Ameliorates Alzheimer's Disease-Associated Neuropathology and Spatial Memory in SAMP8 Mice

2013 ◽  
Vol 38 (3) ◽  
pp. 633-646 ◽  
Author(s):  
Meng-Shan Tan ◽  
Jin-Tai Yu ◽  
Teng Jiang ◽  
Xi-Chen Zhu ◽  
Hua-Shi Guan ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Spatial Memory ◽  
Samp8 Mice

scholarly journals INFLUENCE OF ACUTE PHYSICAL EXERCISE ON COGNITIVE AND MOTOR BEHAVIOR IN AN EXPERIMENTAL MODEL OF ALZHEIMER'S DISEASE

2019 ◽  
Vol 25 (2) ◽  
pp. 152-156
Author(s):  
Meiriélly Furmann ◽  
Denise Barth Rebesco ◽  
Leandro Smouter ◽  
Andressa Panegalli Hosni ◽  
Ivo Ilvan Kerppers ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Physical Exercise ◽  
Size Effect ◽  
Spatial Memory ◽  
Acute Exercise ◽  
Motor Behavior ◽  
Behavioral Alterations ◽  
Intervention Protocol ◽  
Acute Physical Exercise

ABSTRACT Introduction: Aging causes alterations in various executive and cognitive functions, mainly related to the incidence of dementia, especially Alzheimer's disease (AD). Several studies mention physical exercise as a preventive resource for depressive symptoms. Objective: To investigate the cognitive and behavioral alterations related to AD that are capable of slowing disease progression and its complications. Methods: The sample consisted of 10 male Wistar rats, divided into 2 groups (n = 5), swimming and Alzheimer + swimming, with a 6-day intervention protocol. The elevated plus maze test was used to assess anxiety, the Morris water maze for spatial memory, the isolation box for aversive memory, and the open field test to assay motor behavior. Results: There was improvement in spatial memory in the Swimming group (169 ± 142.9 x 24.2 ± 31.3), but motor behavior deteriorated after exercise. An increase in anxious behavior (8 ± 13.03 x 67.8 ± 48.1) was observed in the animals with AD. This is a relevant characteristic of the disease, which did not improve after acute exercise. By analyzing the size effect, it was possible to observe a difference in the Alzheimer + swimming group in terms of reduced anxiety and improved motor behavior after exercise. Despite the benefits of physical exercise for AD symptoms, there is still no consensus on the type of physical exercise and length of intervention necessary to achieve a positive response as a treatment method, since studies are yet to confirm this fact in an acute or chronic manner. Conclusion: Acute physical exercise was not fully effective as a means of treating behavioral alterations related to AD, but had a mean effect on the size effect analysis of motor behavior and anxiety, specifically. Level of evidence IV; Investigation of treatment outcomes.

scholarly journals N-Acetylcysteine Prevents the Spatial Memory Deficits and the Redox-Dependent RyR2 Decrease Displayed by an Alzheimer’s Disease Rat Model

2018 ◽  
Vol 10 ◽  
Author(s):  
Jamileth More ◽  
Nadia Galusso ◽  
Pablo Veloso ◽  
Luis Montecinos ◽  
José Pablo Finkelstein ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Spatial Memory ◽  
Rat Model ◽  
Memory Deficits
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