scholarly journals Dysregulation of Astrocyte–Neuronal Communication in Alzheimer’s Disease

2021 ◽  
Vol 22 (15) ◽  
pp. 7887
Author(s):  
Carmen Nanclares ◽  
Andres Mateo Baraibar ◽  
Alfonso Araque ◽  
Paulo Kofuji

Recent studies implicate astrocytes in Alzheimer’s disease (AD); however, their role in pathogenesis is poorly understood. Astrocytes have well-established functions in supportive functions such as extracellular ionic homeostasis, structural support, and neurovascular coupling. However, emerging research on astrocytic function in the healthy brain also indicates their role in regulating synaptic plasticity and neuronal excitability via the release of neuroactive substances named gliotransmitters. Here, we review how this “active” role of astrocytes at synapses could contribute to synaptic and neuronal network dysfunction and cognitive impairment in AD.

2021 ◽  
pp. 1-16
Author(s):  
Wei Wei ◽  
Yinghua Liu ◽  
Chunling Dai ◽  
Narjes Baazaoui ◽  
Yunn-Chyn Tung ◽  
...  

Background: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by impairments in synaptic plasticity and cognitive performance. Cognitive dysfunction and loss of neuronal plasticity are known to begin decades before the clinical diagnosis of the disease. The important influence of congenital genetic mutations on the early development of AD provides a novel opportunity to initiate treatment during early development to prevent the Alzheimer-like behavior and synaptic dysfunction. Objective: To explore strategies for early intervention to prevent Alzheimer’s disease. Methods: In the present study, we investigated the effect of treatment during early development with a ciliary neurotrophic factor (CNTF) derived peptidergic compound, P021 (Ac-DGGLAG-NH2) on cognitive function and synaptic plasticity in 3xTg-AD transgenic mouse model of AD. 3xTg-AD and genetic background-matched wild type female mice were treated from birth to postnatal day 120 with P021 in diet or as a control with vehicle diet, and cognitive function and molecular markers of neuroplasticity were evaluated. Results: P021 treatment during early development prevented cognitive impairment and increased expressions of pCREB and BDNF that activated downstream various signaling cascades such as PLC/PKC, MEK/ERK and PI3K/Akt, and ameliorated synaptic protein deficit in 4-month-old 3xTg-AD mice. Conclusion: These findings indicate that treatment with the neurotrophic peptide mimetic such as P021 during early development can be an effective therapeutic strategy to rescue synaptic deficit and cognitive impairment in familial AD and related tauopathies.


2017 ◽  
Vol 12 (4) ◽  
pp. 268-285 ◽  
Author(s):  
Nathalie E. Marchand ◽  
Majken K. Jensen

Concern over loss of cognitive function, including descent into Alzheimer’s disease or dementia, grips a growing percentage of men and women worldwide as the global population ages. Many studies, though not all, suggest that maintaining cognitive health, as well as slowing and even preventing cognitive decline, dementia, and Alzheimer’s disease, can be achieved by consuming healthy diets over a long enough period of time. This appears to be the case even for those who initiated dietary changes later in life, as evidenced by an intervention study assessing consumption of a healthy diet among those who were >50 years of age. All such diets share the common traits of being rich in fruits, vegetables, whole grains, and fish or seafood, while also being low in red meat and sweets. A Mediterranean-style diet shares these characteristics and has been associated with an estimated 40% lower risk of cognitive impairment, including mild cognitive impairment, dementia, and Alzheimer’s disease in prospective studies, in addition to being associated with both a 65% lower risk of mild cognitive impairment and improved cognitive performance in a notable randomized controlled trial.


2008 ◽  
Vol 190 (5) ◽  
pp. 1369-1374 ◽  
Author(s):  
Daniella B. Parente ◽  
Emerson L. Gasparetto ◽  
Luiz Celso Hygino da Cruz ◽  
Roberto Cortes Domingues ◽  
Ana Célia Baptista ◽  
...  

Author(s):  
А.В. Иванов ◽  
Э.Д. Вирюс ◽  
В.И. Логинов ◽  
И.С. Зимина ◽  
А.М. Бурдённый ◽  
...  

Моделирование гипергомоцистеинемии на грызунах является одним из основных способов изучения роли гомоцистеина в патофизиологии различных заболеваний (инфаркта миокарда, инсультов, когнитивных нарушений, болезни Альцгеймера, почечной недостаточности и др.). В настоящем обзоре рассмотрены биохимичекие аспекты метаболизма гомоцистеина, генетические способы моделирования гипергомоцистеинемии на крысах и мышах и их влияние на метаболизм как самого гомоцистеина так и на связанные с ним метаболиты: метионин, цистеин, S-аденозилметионин, S-аденозилгомоцистеин. Modeling hyperhomocysteinemia in rodents is a common way to study the role of homocysteine in pathogenesis of various diseases (myocardial infarction, stroke, cognitive impairment, Alzheimer’s disease, kidney failure, etc.). This review focuses on biochemical aspects of homocysteine metabolism, genetic methods for modeling hyperhomocysteinemia in rats and mice, and effects of these models on metabolism of both homocysteine itself and related metabolites (methionine, cysteine, S-adenosylmethionine, S-adenosylhomocysteine).


2020 ◽  
Author(s):  
Chih-Sung Liang ◽  
Kuan-Pin Su ◽  
Chia-Lin Tsai ◽  
Jiunn-Tay Lee ◽  
Che-Sheng Chu ◽  
...  

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