scholarly journals Therapeutic Effect of Yi-Chi-Tsung-Ming-Tang on Amyloidβ1−40-Induced Alzheimer's Disease-Like Phenotype via an Increase of Acetylcholine and Decrease of Amyloidβ

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Chung-Hsin Yeh ◽  
Ming-Tsuen Hsieh ◽  
Chi-Mei Hsueh ◽  
Chi-Rei Wu ◽  
Yi-Chun Huang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Oral Administration ◽  
Learning And Memory ◽  
Neurodegenerative Disorder ◽  
Senile Dementia ◽  
High Dose ◽  
Memory Impairments ◽  
Beneficial Role ◽  
Amyloid Accumulation

Alzheimer's disease (AD) is an irreversible neurodegenerative disorder characterized by amyloid accumulation, neuronal death, and cognitive impairments. Yi-Chi-Tsung-Ming-Tang (YCTMT) is a traditional Chinese medicine and has never been used to enhance cognitive function and treat neurodegenerative disorders such as senile dementia. Whether YCTMT has a beneficial role in improving learning and memory in AD patients remains unclear. The present study showed that oral administration of YCTMT ameliorated amyloid-β- (Aβ1−40) injection-induced learning and memory impairments in rats, examined using passive avoidance and Morris water-maze tests. Immunostaining and Western Blot results showed that continuous Aβ1−40infusion caused amyloid accumulation and decreased acetylcholine level in hippocampus. Oral administration of medium and high dose of YCTMT 7 days after the Aβ1−40infusion decreased amyloid accumulation area and reversed acetylcholine decline in the Aβ1−40-injected hippocampus, suggesting that YCTMT might inhibit Aβplague accumulation and rescue reduced acetylcholine expression. This study has provided evidence on the beneficial role of YCTMT in ameliorating amyloid-induced AD-like symptom, indicating that YCTMT may offer an alternative strategy for treating AD.

scholarly journals Early Hippocampal Sharp-Wave Ripple Deficits Predict Later Learning and Memory Impairments in an Alzheimer’s Disease Mouse Model

Cell Reports ◽  
2019 ◽  
Vol 29 (8) ◽  
pp. 2123-2133.e4 ◽  
Author(s):  
Emily A. Jones ◽  
Anna K. Gillespie ◽  
Seo Yeon Yoon ◽  
Loren M. Frank ◽  
Yadong Huang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Learning And Memory ◽  
Memory Impairments ◽  
Sharp Wave

scholarly journals Effect of Astragaloside IV on Neural Stem Cell Transplantation in Alzheimer’s Disease Rat Models

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Hu Haiyan ◽  
Yang Rensong ◽  
Jin Guoqin ◽  
Zhang Xueli ◽  
Xia Huaying ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Stem Cells ◽  
Stem Cell ◽  
Learning And Memory ◽  
High Dose ◽  
Astragaloside Iv ◽  
Cell Based Therapy ◽  
Proliferation And Differentiation

Stem cell-based therapy is a promising treatment strategy for neurodegenerative diseases such as Alzheimer’s disease (AD). However, the mechanism underlying the maintenance of renewal and replacement capabilities of endogenous progenitor cells or engrafted stem cells in a pathological environment remains elusive. To investigate the effect of astragaloside IV (ASI) on the proliferation and differentiation of the engrafted neural stem cells (NSCs), we cultured NSCs from the hippocampus of E14 rat embryos, treated the cells with ASI, and then transplanted the cells into the hippocampus of rat AD models.In vitroexperimentation showed that 10−5 M ASI induced NSCs to differentiate intoβ-tubulin III+and GFAP+cells. NSCs transplantation into rat AD models resulted in improvements in learning and memory, especially in the ASI-treated groups. ASI treatment resulted in an increase in the number ofβ-tubulin III+cells in the hippocampus. Further investigation showed that ASI inhibited PS1 expressionin vitroandin vivo. The high-dose ASI downregulated the Notch intracellular domain, whereas the low-dose ASI increased Notch-1 and NICD. In conclusion, ASI treatment resulted in improvements in learning and memory of AD models by promoting NSC proliferation and differentiation partly through the Notch signal pathway.

scholarly journals Prostacyclin Promotes Degenerative Pathology in a Model of Alzheimer’s disease

2020 ◽  
Author(s):  
Tasha R. Womack ◽  
Craig Vollert ◽  
Odochi Nwoko ◽  
Monika Schmitt ◽  
Sagi Montazari ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Disorder ◽  
Amyloid Β ◽  
Chronic Neuroinflammation ◽  
Model Of Alzheimer’S Disease ◽  
Amyloid Accumulation ◽  
Prostaglandin H ◽  
The Brain

AbstractAlzheimer’s disease (AD) is a progressive neurodegenerative disorder that is the most common cause of dementia in aged populations. A substantial amount of data demonstrates that chronic neuroinflammation can accelerate neurodegenerative pathologies, while epidemiological and experimental evidence suggests that the use of anti-inflammatory agents may be neuroprotective. In AD, chronic neuroinflammation results in the upregulation of cyclooxygenase and increased production of prostaglandin H2, a precursor for many vasoactive prostanoids. While it is well-established that many prostaglandins can modulate the progression of neurodegenerative disorders, the role of prostacyclin (PGI2) in the brain is poorly understood. We have conducted studies to assess the effect of elevated prostacyclin biosynthesis in a mouse model of AD. Upregulated prostacyclin expression significantly worsened multiple measures associated with amyloid disease pathologies. Mice overexpressing both amyloid and PGI2 exhibited impaired learning and memory and increased anxiety-like behavior compared with non-transgenic and PGI2 control mice. PGI2 overexpression accelerated the development of amyloid accumulation in the brain and selectively increased the production of soluble amyloid-β 42. PGI2 damaged the microvasculature through alterations in vascular length and branching; amyloid expression exacerbated these effects. Our findings demonstrate that chronic prostacyclin expression plays a novel and unexpected role that hastens the development of the AD phenotype.

scholarly journals Comparison Study of Various Nano Technology Formulation of Curcumin in Treatment of Alzheimer’s Disease

2020 ◽  
Vol 8 (3) ◽  
pp. 99-103
Author(s):  
Mahaveer Singh ◽  
Kushali D ◽  
Vinay C H
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Delivery System ◽  
Neurodegenerative Disorder ◽  
Therapeutic Potential ◽  
Senile Dementia ◽  
Molecular Complexes ◽  
Nano Particles ◽  
World Health ◽  
Nano Technology

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder associated with cognitive deterioration affecting day to day living and behavioural activities. It is commonest cause of senile and pre-senile dementia. In Alzheimer’s disease, a peptide referred as amyloid beta aggregates (oligomers), and accumulates in the brain to form deposits called as amyloid plaques. According to the world health organization (WHO), 5% of men and 6% of women of above 60 years are victims with Alzheimer’s type dementia globally. In India prevalence of dementia is 33.6%, of which AD contributes approximately 54% and vascular dementia constitutes approximately 39%. Patients with the prolonged use of some Non-steroidal anti-inflammatory (NSAID) drugs such as ibuprofen have lower risk of developing the symptoms of AD; however the chronic use of NSAID can produce a toxic effect on the kidney, liver and GI tract. Recent studies have demonstrated that a curcumin delivery system based on nanoscience and nanotechnology increases the therapeutic potential of this compound. Specifically, several nano-sized carriers such as phospholipid vesicles (liposomes), micelles, solid lipid nanoparticles, polymeric nanoparticles, emulsions, proteins and other molecular complexes have been developed for the efficient delivery of curcumin. Nano particles have demonstrated the enhanced Bioavailability of curcumin including circulation time in the blood. Various nano technology drug delivery system of curcumin showed increased Bio accessibility during treatment of Alzheimer’s disease.  

P2-450: Hemizygous deletion of synaptojanin1 ameliorates learning and memory impairments in a mouse model of Alzheimer's disease

2010 ◽  
Vol 6 ◽  
pp. e8-e8
Author(s):  
Laura Beth J. McIntire ◽  
Diego Berman ◽  
Jennifer Myaeng ◽  
Agniezka Staniszewski ◽  
Ottavio Arancio ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Learning And Memory ◽  
Memory Impairments ◽  
Hemizygous Deletion ◽  
Model Of Alzheimer’S Disease
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