Cognitive enhancement and neuroprotective effects of Bacopa monnieri in Alzheimer's disease model

2010 ◽  
Vol 127 (1) ◽  
pp. 26-31 ◽  
Author(s):  
Nongnut Uabundit ◽  
Jintanaporn Wattanathorn ◽  
Supaporn Mucimapura ◽  
Kornkanok Ingkaninan
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Enhancement ◽  
Disease Model ◽  
Bacopa Monnieri ◽  
Neuroprotective Effects

scholarly journals PPARγ-coactivator-1α gene transfer reduces neuronal loss and amyloid-β generation by reducing β-secretase in an Alzheimer’s disease model

2016 ◽  
Vol 113 (43) ◽  
pp. 12292-12297 ◽  
Author(s):  
Loukia Katsouri ◽  
Yau M. Lim ◽  
Katrin Blondrath ◽  
Ioanna Eleftheriadou ◽  
Laura Lombardero ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Pyramidal Neurons ◽  
Lentiviral Vector ◽  
Disease Model ◽  
Amyloid Β ◽  
Neuronal Loss ◽  
Peroxisome Proliferator ◽  
Neuroprotective Effects ◽  
Peroxisome Proliferator Activated Receptor

Current therapies for Alzheimer’s disease (AD) are symptomatic and do not target the underlying Aβ pathology and other important hallmarks including neuronal loss. PPARγ-coactivator-1α (PGC-1α) is a cofactor for transcription factors including the peroxisome proliferator-activated receptor-γ (PPARγ), and it is involved in the regulation of metabolic genes, oxidative phosphorylation, and mitochondrial biogenesis. We previously reported that PGC-1α also regulates the transcription of β-APP cleaving enzyme (BACE1), the main enzyme involved in Aβ generation, and its expression is decreased in AD patients. We aimed to explore the potential therapeutic effect of PGC-1α by generating a lentiviral vector to express human PGC-1α and target it by stereotaxic delivery to hippocampus and cortex of APP23 transgenic mice at the preclinical stage of the disease. Four months after injection, APP23 mice treated with hPGC-1α showed improved spatial and recognition memory concomitant with a significant reduction in Aβ deposition, associated with a decrease in BACE1 expression. hPGC-1α overexpression attenuated the levels of proinflammatory cytokines and microglial activation. This effect was accompanied by a marked preservation of pyramidal neurons in the CA3 area and increased expression of neurotrophic factors. The neuroprotective effects were secondary to a reduction in Aβ pathology and neuroinflammation, because wild-type mice receiving the same treatment were unaffected. These results suggest that the selective induction of PGC-1α gene in specific areas of the brain is effective in targeting AD-related neurodegeneration and holds potential as therapeutic intervention for this disease.

scholarly journals Nutrigenomic Studies on the Ameliorative Effect of Enzyme-Digested Phycocyanin in Alzheimer’s Disease Model Mice

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4431
Author(s):  
Yasuyuki Imai ◽  
Yurino Koseki ◽  
Makoto Hirano ◽  
Shin Nakamura
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Oral Administration ◽  
Expression Patterns ◽  
Disease Model ◽  
Neuroprotective Effects ◽  
Aberrant Expression ◽  
Ameliorative Effect

Alzheimer’s disease (AD) is the most common form of dementia, and the cognitive impairments associated with this degenerative disease seriously affect daily life. Nutraceuticals for the prevention or delay of AD are urgently needed. It has been increasingly observed that phycocyanin (PC) exerts neuroprotective effects. AD model mice intracerebroventricularly injected with amyloid beta-peptide 25–35 (Aβ25–35) at 10 nmol/head displayed significant cognitive impairment in the spontaneous alternation test. Cognitive impairment was significantly ameliorated in mice treated with 750 mg/kg of enzyme-digested (ED) PC by daily oral administration for 22 consecutive days. Application of DNA microarray data on hippocampal gene expression to nutrigenomics studies revealed that oral EDPC counteracted the aberrant expression of 35 genes, including Prnp, Cct4, Vegfd (Figf), Map9 (Mtap9), Pik3cg, Zfand5, Endog, and Hbq1a. These results suggest that oral administration of EDPC ameliorated cognitive impairment in AD model mice by maintaining and/or restoring normal gene expression patterns in the hippocampus.

scholarly journals Neuroprotective effects of CD4+CD25+Foxp3+ regulatory T cells in a 3xTg-AD Alzheimer's disease model

Oncotarget ◽  
2016 ◽  
Vol 7 (43) ◽  
pp. 69347-69357 ◽  
Author(s):  
Hyunjung Baek ◽  
Minsook Ye ◽  
Geun-Hyung Kang ◽  
Chanju Lee ◽  
Gihyun Lee ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
T Cells ◽  
Regulatory T Cells ◽  
Disease Model ◽  
Neuroprotective Effects ◽  
Ad Alzheimer’S Disease

Neuroprotective Effects of Apocynin and Galantamine During the Chronic Administration of Scopolamine in an Alzheimer’s Disease Model

2019 ◽  
Vol 70 (2) ◽  
pp. 180-193 ◽  
Author(s):  
Eliezer Joseph ◽  
Daniel Miguel Ángel Villalobos-Acosta ◽  
Mónica Adriana Torres-Ramos ◽  
Eunice Dalet Farfán-García ◽  
Modesto Gómez-López ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Disease Model ◽  
Chronic Administration ◽  
Neuroprotective Effects

Neuroprotective effects of PrxI over-expression in an in vitro human Alzheimer's disease model

2013 ◽  
Vol 114 (3) ◽  
pp. 708-715 ◽  
Author(s):  
Annamaria Cimini ◽  
Roberta Gentile ◽  
Francesco Angelucci ◽  
Elisabetta Benedetti ◽  
Giuseppina Pitari ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Disease Model ◽  
Neuroprotective Effects ◽  
Over Expression

Nutritional aspects and their influences on the pathophysiology of

2014 ◽  
Vol 23 (1) ◽  
pp. 33
Author(s):  
Nathalia Liberato Nascimento ◽  
Iwyson Henrique Fernandes da Costa ◽  
Rivelilson Mendes de Freitas
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Fatty Acids ◽  
Folic Acid ◽  
Saturated Fatty Acids ◽  
Free Radical Scavengers ◽  
Radical Scavengers ◽  
High Intake ◽  
Neuroprotective Effects ◽  
Nutritional Factors

The objective of this study was to conduct a review about the nutritional aspects and their influences on the pathophysiology of Alzheimer’s disease. The review describes the pathophysiology of Alzheimer’s disease, the generally indicated diets, and the nutritional factors that may aggravate the disease based on a literature review using the following keywords in English and Portuguese: “Alzheimer’s disease”, “physiopathology”, “nutritional aspects”, and “antioxidants”. A total of 100 articles were found, 48 in Lilacs and 52 in MedLine, but only 54 articles were selected for the review. The use of antioxidants as free radical scavengers is generally indicated in diets for Alzheimer’s patients. Studies also suggest that caffeine, vitamin B12, and folic acid have neuroprotective effects. Cohort studies found that a high intake of saturated fatty acids and obesity increase the risk of Alzheimer’s disease. People with Alzheimer’s disease should avoid diets high in carbohydrates and saturated fats, and prefer foods high in antioxidants.Keywords: Alzheimer disease; Antioxidants; Neurophysiology; Review literture as topic.

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