scholarly journals FcγRIIb mediates amyloid-β neurotoxicity and memory impairment in Alzheimer’s disease

2013 ◽  
Vol 123 (7) ◽  
pp. 2791-2802 ◽  
Author(s):  
Tae-In Kam ◽  
Sungmin Song ◽  
Youngdae Gwon ◽  
Hyejin Park ◽  
Ji-Jing Yan ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Memory Impairment ◽  
Amyloid Β

Melatonin Attenuates Memory Impairment, Amyloid-β Accumulation, and Neurodegeneration in a Rat Model of Sporadic Alzheimer’s Disease

2015 ◽  
Vol 47 (1) ◽  
pp. 103-116 ◽  
Author(s):  
Ekaterina A. Rudnitskaya ◽  
Natalia A. Muraleva ◽  
Kseniya Yi. Maksimova ◽  
Elena Kiseleva ◽  
Nataliya G. Kolosova ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Rat Model ◽  
Memory Impairment ◽  
Amyloid Β ◽  
Sporadic Alzheimer’S Disease

scholarly journals Treadmill exercise improves memory and increases hippocampal BDNF in a rat model of Alzheimer's Disease

2020 ◽  
Vol 24 (4) ◽  
pp. 250-256
Author(s):  
Rokhsareh Abshenas ◽  
◽  
Tayebe Artimani ◽  
Iraj Amiri ◽  
Siamak Shahidi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Avoidance Learning ◽  
Memory Impairment ◽  
Treadmill Exercise ◽  
Amyloid Β ◽  
Male Rats ◽  
Bdnf Expression ◽  
Learning Tasks ◽  
Model Of Alzheimer’S Disease

Introduction: Alzheimer’s disease is strongly correlated with learning and memory impairments. As exercise can enhance memory and learning, in this study, we have investigated the effects of treadmill exercise on memory impairment in amyloid β (Aβ)- treated rats focusing on brain-derived neurotrophic factor (BDNF) expression. Methods: Wistar male rats received intracerebroventricular (ICV) injection of Aβ and exercised on a treadmill for one month. Memory function was assessed using Morris water maze (MWM) and avoidance learning tasks. The level of BDNF was examined by the ELISA test. Results: The results of MWM and avoidance learning tasks showed that treadmill exercise could improve Aβ- induced memory impairment significantly. Moreover, BDNF expression increased following exercise in the Aβ- treated rats. Conclusion: The present results suggested that treadmill exercise may improve memory in Alzheimer’s disease by increasing BDNF level in the hippocampus.

scholarly journals Visuospatial memory impairment as a potential neurocognitive marker to predict tau pathology in Alzheimer’s continuum

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Eun Hyun Seo ◽  
Ho Jae Lim ◽  
Hyung-Jun Yoon ◽  
Kyu Yeong Choi ◽  
Jang Jae Lee ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Medial Temporal Lobe ◽  
Memory Impairment ◽  
Prediction Models ◽  
Characteristic Curve ◽  
Amyloid Β ◽  
Tau Pathology ◽  
Discrimination Ability

Abstract Background Given that tau accumulation, not amyloid-β (Aβ) burden, is more closely connected with cognitive impairment in Alzheimer’s disease (AD), a detailed understanding of the tau-related characteristics of cognitive function is critical in both clinical and research settings. We investigated the association between phosphorylated tau (p-Tau) level and cognitive impairment across the AD continuum and the mediating role of medial temporal lobe (MTL) atrophy. We also developed a prediction model for abnormal tau accumulation. Methods We included participants from the Gwangju Alzheimer’s Disease and Related Dementia Cohort in Korea, who completed cerebrospinal fluid analysis and clinical evaluation, and corresponded to one of three groups according to the biomarkers of A and T profiles based on the National Institute on Aging and Alzheimer’s Association research framework. Multiple linear and logistic regression analyses were performed to examine the association between p-Tau and cognition and to develop prediction models. Receiver operating characteristic curve analysis was performed to examine the discrimination ability of the models. Results Among 185 participants, 93 were classified as A-T-, 23 as A+T-, and 69 as A+T+. There was an association between decreased visuospatial delayed memory performance and p-Tau level (B = − 0.754, β = − 0.363, p < 0.001), independent of other relevant variables (e.g., Aβ). MTL neurodegeneration was found to mediate the association between the two. Prediction models with visuospatial delayed memory alone (area under the curve [AUC] = 0.872) and visuospatial delayed memory and entorhinal thickness (AUC = 0.921) for abnormal tau accumulation were suggested and they were validated in an independent sample (AUC = 0.879 and 0.891, respectively). Conclusion It is crucial to identify sensitive cognitive measures that capture subtle cognitive impairment associated with underlying pathological changes. Preliminary findings from the current study might suggest that abnormal tau accumulation underlies episodic memory impairment, particularly visuospatial modality, in the AD continuum. Suggested models are potentially useful in predicting tau pathology, and might be utilized practically in the field.

Tooth Loss Induces Memory Impairment and Gliosis in App Knock-In Mouse Models of Alzheimer’s Disease

2021 ◽  
Vol 80 (4) ◽  
pp. 1687-1704
Author(s):  
Ferdous Taslima ◽  
Cha-Gyun Jung ◽  
Chunyu Zhou ◽  
Mona Abdelhamid ◽  
Mohammad Abdullah ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mrna Expression ◽  
Neuronal Activity ◽  
Memory Impairment ◽  
Tooth Loss ◽  
Amyloid Β ◽  
Glial Activation ◽  
Expression Levels ◽  
Mrna Expression Levels

Background: Epidemiological studies have shown that tooth loss is associated with Alzheimer’s disease (AD) and dementia. However, the molecular and cellular mechanisms by which tooth loss causes AD remain unclear. Objective: We investigated the effects of tooth loss on memory impairment and AD pathogenesis in AppNL-G-F mice. Methods: Maxillary molar teeth on both sides were extracted from 2-month-old AppNL-G-F mice, and the mice were reared for 2 months. The short- and long-term memory functions were evaluated using a novel object recognition test and a passive avoidance test. Amyloid plaques, amyloid-β (Aβ) levels, glial activity, and neuronal activity were evaluated by immunohistochemistry, Aβ ELISA, immunofluorescence staining, and western blotting. The mRNA expression levels of neuroinflammatory cytokines were determined by qRT-PCR analysis. Results: Tooth loss induced memory impairment via an amyloid-cascade-independent pathway, and decreased the neuronal activity, presynaptic and postsynaptic protein levels in both the cortex and hippocampus. Interestingly, we found that tooth loss induced glial activation, which in turn leads to the upregulation of the mRNA expression levels of the neuroinflammation cytokines tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and IL-1β in the hippocampus. We also found that tooth loss activated a stress-activated protein kinase, c-Jun N-terminal kinase (JNK), and increased heat shock protein 90 (HSP90) levels in the hippocampus, which may lead to a glial activation. Conclusion: Our findings suggest that taking care of teeth is very important to preserve a healthy oral environment, which may reduce the risk of cognitive dysfunction.

Neoline Improves Memory Impairment and Reduces Amyloid-β Level and Tau Phosphorylation Through AMPK Activation in the Mouse Alzheimer’s Disease Model

2021 ◽  
pp. 1-10
Author(s):  
Quan Feng Liu ◽  
Suganya Kanmani ◽  
Jinhyuk Lee ◽  
Geun-Woo Kim ◽  
Songhee Jeon ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Memory Impairment ◽  
Amyloid Β ◽  
Chronic Administration ◽  
Therapeutic Effects ◽  
Ampk Activation ◽  
The Brain ◽  
Ad Mouse Model

Background: Alzheimer’s disease (AD) is the most general, chronic, and progressive neurodegenerative senile disorder characterized clinically by progressive cognitive deterioration and memory impairment. Neoline is effective against neuropathic pain models, but the effects of neoline against AD-like phenotypes have not been investigated. Objective: We offer the investigation of the effects of neoline in AD. Methods: In this study, a Tg-APPswe/PS1dE9 AD mouse model was treated orally with neoline at a concentration of 0.5 mg/kg or 0.1 mg/kg starting at 7.5 months and administered for three months, and its anti-AD effects were evaluated. Results: Neoline improved memory and cognition impairments and reduced the number of amyloid-beta plaque and the amount of amyloid-β in the brain of AD mice. Furthermore, neoline reduced the anxiety behavior in the AD mouse model. The chronic administration of neoline also induced AMPK phosphorylation and decreased tau, amyloid-β, and BACE1 expression in the hippocampus. These findings indicate that chronic administration of neoline has therapeutic effects via AMPK activation, and BACE1 downregulation resulted in a decrease in the amyloid-β levels in the brain of Tg-APPswe/PS1dE9 AD mice. Conclusion: Our results suggest that neoline is a therapeutic agent for the cure of neurodegenerative diseases like AD.

scholarly journals Effects of GrandFusion Diet on Cognitive Impairment in Transgenic Mouse Model of Alzheimer’s Disease

Nutrients ◽  
2020 ◽  
Vol 13 (1) ◽  
pp. 117 ◽  
Author(s):  
Jin Yu ◽  
Hong Zhu ◽  
Saeid Taheri ◽  
William Mondy ◽  
Stephen Perry ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Cathepsin B ◽  
Memory Impairment ◽  
Chronic Traumatic Encephalopathy ◽  
Disease Process ◽  
Amyloid Β ◽  
Aβ Peptide ◽  
Model Of Alzheimer’S Disease

Alzheimer’s disease (AD) is the result of the deposition of amyloid β (Aβ) peptide into amyloid fibrils and tau into neurofibrillary tangles. At the present time, there are no possible treatments for the disease. We have recently shown that diets enriched in phytonutrients show protection or limit the extent of damage in a number of neurological disorders. GrandFusion (GF) diets have attenuated the outcomes in animal models of traumatic brain injury, cerebral ischemia, and chronic traumatic encephalopathy. In this study, we investigated the effect of GF diets in a mouse model of AD prior to the development of amyloid plaques to show how this treatment paradigm would alter the accumulation of Aβ peptide and related pathologic changes (i.e., inflammation, cathepsin B, and memory impairment). Administration of GF diets (2–4%) over a period of four months in APP/ΔPS1 double-transgenic mice resulted in attenuation in Aβ peptide levels, reduction of amyloid load, and inflammation, increased cathepsin B expression, and improved spatial orientation. Additionally, treatment with GF diets increased nerve growth factor (NGF) levels in the brain and tempered the memory impairment in the animal model. These data suggest that GF diets may alter the development and progression of the mechanisms associated with the disease process to effectively modify AD pathogenesis.

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