scholarly journals Case Series Using Montelukast in Patients with Memory Loss and Dementia

2017 ◽  
Vol 11 (1) ◽  
pp. 7-10 ◽  
Author(s):  
Spencer I. Rozin

Cognitive decline and dementia are a growing problem as the population ages. Effective therapies to prevent and treat these problems are limited. Neuro-inflammation has been suggested as a cause of dementia [1]. Montelukast is a leukotriene receptor antagonist used to treat seasonal allergies and asthma. It acts as a cysteinyl leukotriene (CysLT1) receptor antagonist blocking the action of leukotrienes and decreasing inflammation [2]. Animal studies have shown that administering Montelukast improves memory function [3]. This case series of patients in a private Internal Medicine practice between 2013-2014 used Montelukast in patients with various levels of memory impairment and dementia. Patients were given Montelukast 80 mg daily in 4 divided doses every 2-3 hours. Memory impaired patients had subjective improvement in the memory and recall. Patients with dementia were noted by family members to be less agitated, but had no memory improvement at the doses used. Montelukast may be useful to treat memory impairment and dementia. Long term use might act as a prophylactic to prevent dementia.

2020 ◽  
Author(s):  
Nicholas Don-Doncow ◽  
Frank Matthes ◽  
Hana Matuskova ◽  
Sara Rattik ◽  
Lotte Vanherle ◽  
...  

AbstractBackground and PurposeMetabolic and cardiovascular disease is the most prevalent disease burden in the world and risk factor for progressive cognitive decline. Evidence associates cardiovascular risk factors to unfavorable systemic and neuro-inflammation and to cognitive decline. Cardiovascular therapeutics (e.g., statins and antihypertensives) possess immune-modulatory functions in parallel to their cholesterol- or blood pressure (BP)-lowering properties. How their ability to modify immune responses affects cognitive function is unknown.Experimental ApproachBy using flow cytometry, Elisa, qPCR, Western blotting and object recognition tasks, we examined the effect of chronic hypercholesterolemia on inflammation and memory function in Apolipoprotein E (ApoE) knockout mice and normocholesterolemic wild-type mice.Key resultsChronic hypercholesterolemia associated to moderate BP elevations and apparent immune system activation characterized by increases in circulating pro-inflammatory Ly6Chi monocytes in ApoE-/- mice. The persistent low-grade immune activation associated to chronic hypercholesterolemia facilitates the infiltration of pro-inflammatory Ly6Chi monocytes into the brain of aged ApoE-/- but not wild-type mice, linking to memory dysfunction. Therapeutic administration of cholesterol-lowering simvastatin reduced BP, systemic and neuro-inflammation, and the occurrence of memory deficits in aged ApoE-/- mice. BP-lowering therapy alone (i.e. hydralazine) attenuated some neuro-inflammatory signatures but not the occurrence of memory deficits. When administered in combination, it reduced effectiveness of statin therapy in some instances.Conclusions and ImplicationsOur study suggests a link between chronic hypercholesterolemia, myeloid cell activation and neuro-inflammation with memory impairment. Cholesterol-lowering therapy provides effectiveness to attenuate memory impairment and inflammatory events and hence, emerges as safe therapeutic strategy to control hypercholesterolemia-associated memory decline.What is already knowncardiovascular risk factors link to unfavorable systemic and neuro-inflammation and to cognitive declinecardiovascular therapeutics possess immune-modulatory functions in parallel to their principle cholesterol- or blood pressure-lowering propertiesWhat this study addslinks chronic hypercholesterolemia in mice to specific immune responses and the development of memory impairmentfavorable outcomes in respect to neuro-inflammation and memory function in hypercholesterolemic mice after statin therapyClinical significanceopens the door for available CVD therapeutics with long-term safety profiles to managing cognitive dysfunctiontargeted monitoring of inflammatory signature in patients with high cardiovascular burden (surrogate biomarker of cognitive decline)


Foods ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 221
Author(s):  
Do-Youn Jeong ◽  
Myeong Seon Ryu ◽  
Hee-Jong Yang ◽  
Sunmin Park

Fermented soybean paste is an indigenous food for use in cooking in East and Southeast Asia. Korea developed and used its traditional fermented foods two thousand years ago. Chungkookjang has unique characteristics such as short-term fermentation (24–72 h) without salt, and fermentation mostly with Bacilli. Traditionally fermented chungkookjang (TFC) is whole cooked soybeans that are fermented predominantly by Bacillus species. However, Bacillus species are different in the environment according to the regions and seasons due to the specific bacteria. Bacillus species differently contribute to the bioactive components of chungkookjang, resulting in different functionalities. In this review, we evaluated the production process of poly-γ-glutamic acid (γ-PGA)-rich chungkookjang fermented with specific Bacillus species and their effects on memory function through the modulation of brain insulin resistance, neuroinflammation, and the gut–microbiome–brain axis. Bacillus species were isolated from the TFC made in Sunchang, Korea, and they included Bacillus (B.) subtilis, B. licheniformis, and B. amyloliquefaciens. Chungkookjang contains isoflavone aglycans, peptides, dietary fiber, γ-PGA, and Bacillus species. Chungkookjangs made with B. licheniformis and B. amyloliquefaciens have higher contents of γ-PGA, and they are more effective for improving glucose metabolism and memory function. Chungkookjang has better efficacy for reducing inflammation and oxidative stress than other fermented soy foods. Insulin sensitivity is improved, not only in systemic organs such as the liver and adipose tissues, but also in the brain. Chungkookjang intake prevents and alleviates memory impairment induced by Alzheimer’s disease and cerebral ischemia. This review suggests that the intake of chungkookjang (20–30 g/day) rich in γ-PGA acts as a synbiotic in humans and promotes memory function by suppressing brain insulin resistance and neuroinflammation and by modulating the gut–microbiome–brain axis.


2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Gil-Yong Lee ◽  
Chan Lee ◽  
Gyu Hwan Park ◽  
Jung-Hee Jang

Increasing evidence suggests that neurodegenerative disorders such as Alzheimer’s disease (AD) are mediated via disruption of cholinergic neurons and enhanced oxidative stress. Therefore, attention has been focused on searching for antioxidant phytochemicals for the prevention and/or treatment of AD through their ability to fortify cholinergic function and antioxidant defense capacity. In this study, we have investigated the neuroprotective effect ofα-pinene (APN) against learning and memory impairment induced by scopolamine (SCO, 1 mg/kg, i.p.), a muscarinic receptor antagonist in C57BL/6 mice. Administration of APN (10 mg/kg, i.p.) significantly improved SCO-induced cognitive dysfunction as assessed by Y-maze and passive avoidance tests. In Morris water-maze test, APN effectively shortened the mean escape latency to find the hidden platform during training days. To further elucidate the molecular mechanisms underlying the neuroprotective effect of APN, the expression of proteins involved in the acetylcholine metabolism and antioxidant system was examined. Particularly, APN treatment increased mRNA expression of choline acetyltransferase in the cortex and protein levels of antioxidant enzymes such as heme oxygenase-1 and manganese superoxide dismutase in the hippocampus via activation of NF-E2-related factor 2. These findings suggest the possible neuroprotective potentials of APN for the management of dementia with learning and memory loss.


2012 ◽  
Vol 31 (1) ◽  
pp. 101-111 ◽  
Author(s):  
Yanyong Liu ◽  
Haji Akber Aisa ◽  
Chao Ji ◽  
Nan Yang ◽  
Haibo Zhu ◽  
...  

Aging-associated cognitive impairment is an important health care issue since individuals with mild cognitive impairment are more likely to develop Alzheimer’s disease. In the present study, the protective effect of Gossypium herbaceam extracts (GHE) on learning and memory impairment associated with aging were examined in vivo using Morris water maze and step through task. Furthermore, the antioxidant activity and neuroprotective effect of GHE was investigated with methods of histochemistry and biochemistry. These data showed that oral administration with GHE at the doses of 35, 70, and 140 mg/kg exerted an improved effect on the learning and memory impairment in aged rats. Subsequently, GHE afforded a beneficial action on eradication of free radicals without influence on the activity of glutathione peroxidase and superoxide dismutase. GHE treatment enhanced the expression levels of nerve growth factor. Meanwhile, proliferation of neural progenitor cells was elevated in hippocampus after treatment with GHE. Taken together, neurogenic niche improvement could be involved in the mechanism underlying neuroprotection of GHE against aging-associated cognitive impairment. These findings suggested that GHE might be a potential agent as cognitive-enhancing drugs that delay or halt mild cognitive impairment progression to Alzheimer’s disease or treatment of aging-associated cognitive impairment.


2021 ◽  
Vol 13 ◽  
Author(s):  
Wei Zhang ◽  
Tianhao Zhang ◽  
Tingting Pan ◽  
Shilun Zhao ◽  
Binbin Nie ◽  
...  

Objectives: Neuropsychological tests are an important basis for the memory impairment diagnosis in Alzheimer’s disease (AD). However, multiple memory tests might be conflicting within-subjects and lead to uncertain diagnoses in some cases. This study proposed a framework to diagnose the uncertain cases of memory impairment.Methods: We collected 2,386 samples including AD, mild cognitive impairment (MCI), and cognitive normal (CN) using 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) and three different neuropsychological tests (Mini-Mental State Examination, Alzheimer’s Disease Assessment Scale-Cognitive Subscale, and Clinical Dementia Rating) from the Alzheimer’s Disease Neuroimaging Initiative (ADNI). A deep learning (DL) framework using FDG-PET was proposed to diagnose uncertain memory impairment cases that were conflicting between tests. Subsequent ANOVA, chi-squared, and t-test were used to explain the potential causes of uncertain cases.Results: For certain cases in the testing set, the proposed DL framework outperformed other methods with 95.65% accuracy. For the uncertain cases, its positive diagnoses had a significant (p < 0.001) worse decline in memory function than negative diagnoses in a longitudinal study of 40 months on average. In the memory-impaired group, uncertain cases were mainly explained by an AD metabolism pattern but mild in extent (p < 0.05). In the healthy group, uncertain cases were mainly explained by a non-energetic mental state (p < 0.001) measured using a global deterioration scale (GDS), with a significant depression-related metabolism pattern detected (p < 0.05).Conclusion: A DL framework for diagnosing uncertain cases of memory impairment is proposed. Proved by longitudinal tracing of its diagnoses, it showed clinical validity and had application potential. Its valid diagnoses also provided evidence and explanation of uncertain cases based on the neurodegeneration and depression mental state.


2020 ◽  
Vol 6 (33) ◽  
pp. eabb9036
Author(s):  
Bradlee L. Heckmann ◽  
Brett J. W. Teubner ◽  
Emilio Boada-Romero ◽  
Bart Tummers ◽  
Clifford Guy ◽  
...  

Noncanonical functions of autophagy proteins have been implicated in neurodegenerative conditions, including Alzheimer’s disease (AD). The WD domain of the autophagy protein Atg16L is dispensable for canonical autophagy but required for its noncanonical functions. Two-year-old mice lacking this domain presented with robust β-amyloid (Aβ) pathology, tau hyperphosphorylation, reactive microgliosis, pervasive neurodegeneration, and severe behavioral and memory deficiencies, consistent with human disease. Mechanistically, we found this WD domain was required for the recycling of Aβ receptors in primary microglia. Pharmacologic suppression of neuroinflammation reversed established memory impairment and markers of disease pathology in this novel AD model. Therefore, loss of the Atg16L WD domain drives spontaneous AD in mice, and inhibition of neuroinflammation is a potential therapeutic approach for treating neurodegeneration and memory loss. A decline in expression of ATG16L in the brains of human patients with AD suggests the possibility that a similar mechanism may contribute in human disease.


2019 ◽  
Vol 148 ◽  
pp. 109-117
Author(s):  
Alireza Gharib ◽  
Alireza Komaki ◽  
Hamed Manoochehri Khoshinani ◽  
Massoud Saidijam ◽  
Victoria Barkley ◽  
...  

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