Synergistic effects of an innovative combination therapy on treating Alzheimer's disease involving modulation of gut dysbiosis

2020 ◽  
Vol 16 (S9) ◽  
Author(s):  
Feng‐Shiun Shie ◽  
Chia‐Yu Hsu ◽  
Po‐Kuan Chao ◽  
Jung‐Tsung Hsueh ◽  
John Tsu‐An Hsu ◽  
...  
2003 ◽  
Vol 5 (3) ◽  
pp. 299-305

Alzheimer's disease is a progressive, debilitating form of dementia affecting more than 18 million people worldwide. Without a cure, many patients and their families must turn to long-term care institutions during the later stages of the disease. Our current treatments only delay progression and help control behavioral symptoms. In recent years, research within this field has expanded to include many clinical trials on potential drug therapies. However, despite the numerous studies, the enigma of this disease remains. It is difficult yet necessary, to stay abreast of emerging information that may warrant changes in current therapy. Rationale for combination therapy becomes evident as we review the multiple neurochemical pathways common to the disease. This paper will review available information on Alzheimer's disease pharmacotherapy, and evaluate data on the use of combination drug therapy. Individual efficacy, possible synergistic effects, and the safety of combination therapy will also be addressed.


2020 ◽  
Vol 57 (12) ◽  
pp. 5026-5043 ◽  
Author(s):  
Shan Liu ◽  
Jiguo Gao ◽  
Mingqin Zhu ◽  
Kangding Liu ◽  
Hong-Liang Zhang

Abstract Understanding how gut flora influences gut-brain communications has been the subject of significant research over the past decade. The broadening of the term “microbiota-gut-brain axis” from “gut-brain axis” underscores a bidirectional communication system between the gut and the brain. The microbiota-gut-brain axis involves metabolic, endocrine, neural, and immune pathways which are crucial for the maintenance of brain homeostasis. Alterations in the composition of gut microbiota are associated with multiple neuropsychiatric disorders. Although a causal relationship between gut dysbiosis and neural dysfunction remains elusive, emerging evidence indicates that gut dysbiosis may promote amyloid-beta aggregation, neuroinflammation, oxidative stress, and insulin resistance in the pathogenesis of Alzheimer’s disease (AD). Illustration of the mechanisms underlying the regulation by gut microbiota may pave the way for developing novel therapeutic strategies for AD. In this narrative review, we provide an overview of gut microbiota and their dysregulation in the pathogenesis of AD. Novel insights into the modification of gut microbiota composition as a preventive or therapeutic approach for AD are highlighted.


2015 ◽  
Vol 6 (1) ◽  
pp. 55-57 ◽  
Author(s):  
Daniel Kamp ◽  
Myrella Paschali ◽  
Tillmann Supprian ◽  
Christian Lange-Asschenfeldt

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 690
Author(s):  
Umair Shabbir ◽  
Muhammad Sajid Arshad ◽  
Aysha Sameen ◽  
Deog-Hwan Oh

The gut microbiota (GM) represents a diverse and dynamic population of microorganisms and about 100 trillion symbiotic microbial cells that dwell in the gastrointestinal tract. Studies suggest that the GM can influence the health of the host, and several factors can modify the GM composition, such as diet, drug intake, lifestyle, and geographical locations. Gut dysbiosis can affect brain immune homeostasis through the microbiota–gut–brain axis and can play a key role in the pathogenesis of neurodegenerative diseases, including dementia and Alzheimer’s disease (AD). The relationship between gut dysbiosis and AD is still elusive, but emerging evidence suggests that it can enhance the secretion of lipopolysaccharides and amyloids that may disturb intestinal permeability and the blood–brain barrier. In addition, it can promote the hallmarks of AD, such as oxidative stress, neuroinflammation, amyloid-beta formation, insulin resistance, and ultimately the causation of neural death. Poor dietary habits and aging, along with inflammatory responses due to dysbiosis, may contribute to the pathogenesis of AD. Thus, GM modulation through diet, probiotics, or fecal microbiota transplantation could represent potential therapeutics in AD. In this review, we discuss the role of GM dysbiosis in AD and potential therapeutic strategies to modulate GM in AD.


2016 ◽  
Vol 12 (5) ◽  
pp. 623-630 ◽  
Author(s):  
James A. Hendrix ◽  
Randall J. Bateman ◽  
H. Robert Brashear ◽  
Cynthia Duggan ◽  
Maria C. Carrillo ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Tadashi Kanamori ◽  
Yoshiyuki Kaneko ◽  
Kouju Yamada ◽  
Masahiro Suzuki

Pica in Alzheimer's disease (AD) makes it difficult for caregivers to provide care. However, few effective medications have been reported for pica in AD. We report a case of AD with pica that was successfully improved by trazodone and fluvoxamine. An 80-year-old woman with AD was admitted to our hospital due to aggravated pica, including eating weeds in the facility's garden and eating a dishwashing sponge. Her pica was accompanied by oral tendency, prosopagnosia, and placidity. She took rivastigmine and memantine, but these were ineffective for her pica. She was given olanzapine and perospirone, but both were discontinued due to over-sedation and severe extrapyramidal symptoms, respectively. We then administered trazodone and fluvoxamine, both of which have demonstrated effectiveness for pica in frontotemporal dementia (FTD). Her pica behaviors then disappeared without daytime sleepiness. In this case, pica with oral tendency, which was accompanied by prosopagnosia and placidity, may be interpreted as a partial symptom of Klüver–Bucy syndrome (KBS). KBS is often seen in FTD, but also occurs in late-stage AD. Our case together with previous reports showing that trazodone and fluvoxamine were effective for pica in FTD suggest that the same common drug therapy may be successful in pica with oral tendency, regardless of the subtype of dementia.


2011 ◽  
Vol 6 (4) ◽  
pp. 228
Author(s):  
José L Molinuevo ◽  

Two effective symptomatic therapies are available for Alzheimer’s disease: the cholinesterase inhibitors (ChEIs) and memantine, an N-methyl-D-aspartate receptor antagonist. Current data demonstrate that combination therapy with memantine and a ChEI produces symptomatic benefits in all domains of AD. The benefits of combination therapy are greater than those of ChEI monotherapy, are sustained long term and appear to increase with time.


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