Memantine ameliorates learning and memory disturbance and the behavioral and psychological symptoms of dementia in thiamine-deficient mice

Makino, Mitsuhiro; Takahashi-Ito, Kaori; Murasawa, Hiroyasu; Pawlak, Akiko; Kashimoto, Yoshinori; Kitano, Yutaka

doi:10.1016/j.pbb.2019.05.008

Cited by 6 publications

(6 citation statements)

References 46 publications

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“…One day after the Y-maze test, the PA test was carried out for evaluating long-term memory with some modifications 78 ( Figures 3 , 4 , and S4 ). The apparatus consisted of dark (240 mm width, 245 mm depth, 300 mm height) chamber with grid floors and a light (100 mm width, 100 mm depth, 300 mm height) chamber.…”

Section: Methodsmentioning

confidence: 99%

Identification of Faecalibacterium prausnitzii strains for gut microbiome-based intervention in Alzheimer’s-type dementia

Ueda

Shinkai

Shiroma

et al. 2021

Cell Reports Medicine

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Evidence linking the gut-brain axis to Alzheimer's disease (AD) is accumulating, but the characteristics of causally important microbes are poorly understood. We perform a fecal microbiome analysis in healthy subjects and those with mild cognitive impairment (MCI) and AD. We find that Faecalibacterium prausnitzii (F. prausnitzii) correlates with cognitive scores and decreases in the MCI group compared with the healthy group. Two isolated strains from the healthy group, live Fp360 and pasteurized Fp14, improve cognitive impairment in an AD mouse model. Whole-genome comparison of isolated strains reveals specific orthologs that are found only in the effective strains and are more abundant in the healthy group compared with the MCI group. Metabolome and RNA sequencing analyses of mouse brains provides mechanistic insights into the relationship between the efficacy of pasteurized Fp14, oxidative stress, and mitochondrial function. We conclude that F. prausnitzii strains with these specific orthologs are candidates for gut microbiome-based intervention in Alzheimer's-type dementia.

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Section: Methodsmentioning

confidence: 99%

Identification of Faecalibacterium prausnitzii strains for gut microbiome-based intervention in Alzheimer’s-type dementia

Ueda

Shinkai

Shiroma

et al. 2021

Cell Reports Medicine

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“…One of the limitations of this study was the failure to examine the TD-induced immediate effects on neurobehaviors during the feeding period. As suggested by previous publications, some of the TD-induced deficits, such as loss of motor coordination [ 38 ] and impaired learning and memory [ 34 , 70 ], were observed during or immediately after the feeding period. It may also be of interest to determine the immediate effects of TD on locomotion and anxiety.…”

Section: Discussionmentioning

confidence: 83%

“…TD rats showed enduring impairment in passive avoidance learning [ 15 , 22 , 62 ], the water maze task [ 66 , 67 ], and the T-maze test [ 15 , 68 , 69 ]. In mice, the impairment of learning and memory was observed during the period animals were fed a TD diet, suggesting an acute effect of TD [ 34 , 70 ]. More severe approaches, such as a TD diet in combination with either pyrithiamine [ 38 ] or chronic alcohol drinking [ 71 ], could produce long-term memory impairments in mice.…”

Section: Discussionmentioning

confidence: 99%

Thiamine Deficiency Causes Long-Lasting Neurobehavioral Deficits in Mice

Wen

et al. 2020

Brain Sciences

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Thiamine deficiency (TD) has detrimental effects on brain health and neurobehavioral development, and it is associated with many aging-related neurological disorders. To facilitate TD-related neuropsychological studies, we generated a TD mouse model by feeding a thiamine-deficient diet for 30 days, followed by re-feeding the control diet for either one week or 16 weeks as recovery treatment. We then performed neurobehavioral tests in these two cohorts: cohort of one week post TD treatment (1 wk-PTDT) and 16 weeks post TD treatment (16 wks-PTDT). The TD mice showed no significant difference from control in any tests in the 1 wk-PTDT cohort at the age of 13–14 weeks. The tests for the 16 wks-PTDT cohort at the age of 28–29 weeks, however, demonstrated anxiety and reduced locomotion in TD animals in open field and elevated plus maze. In comparison, rotor rod and water maze revealed no differences between TD and control mice. The current findings of the differential effects of the same TD treatment on locomotion and anxiety at different ages may reflect the progressive and moderate change of TD-induced neurobehavioral effects. The study suggests that, even though the immediate neurobehavioral impact of TD is modest or negligible at a young age, the impact could develop and become severe during the aging process.

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“…In support of the proposed astrocyte glutamate excitotoxicity hypothesis, Makino et al. (2019) reported that memory impairment and anxiogenic effects induced by thiamine deficiency in mice are blocked by memantine, an NMDAR antagonist which suppresses glutamate excitotoxicity. Thiamine deficiency also affects oligodendrocytes (leading to demyelination) (Langlais and Zhang, 1997; Chatterton et al., 2020).…”

Section: Appendix E – Background Information On Thiamine Deficiencymentioning

confidence: 91%

Follow‐up of the re‐evaluation of sulfur dioxide (E 220), sodium sulfite (E 221), sodium bisulfite (E 222), sodium metabisulfite (E 223), potassium metabisulfite (E 224), calcium sulfite (E 226), calcium bisulfite (E 227) and potassium bisulfite (E 228)

Younes¹,

Aquilina²,

Castle³

et al. 2022

EFS2

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Sulfur dioxide–sulfites (E 220–228) were re‐evaluated in 2016, resulting in the setting of a temporary ADI of 0.7 mg SO2 equivalents/kg bw per day. Following a European Commission call for data, the present follow‐up opinion assesses data provided by interested business operators (IBOs) and additional evidence identified in the publicly available literature. No new biological or toxicological data addressing the data gaps described in the re‐evaluation were submitted by IBOs. Taking into account data identified from the literature search, the Panel concluded that there was no substantial reduction in the uncertainties previously identified in the re‐evaluation. Therefore, the Panel considered that the available toxicity database was inadequate to derive an ADI and withdrew the current temporary group acceptable daily intake (ADI). A margin of exposure (MOE) approach was considered appropriate to assess the risk for these food additives. A lower confidence limit of the benchmark dose of 38 mg SO2 equivalents/kg bw per day, which is lower than the previous reference point of 70 mg SO2 equivalents/kg bw per day, was estimated based on prolonged visual evoked potential latency. An assessment factor of 80 was applied for the assessment of the MoE. At the estimated dietary exposures, when using a refined exposure scenario (Data set D), MOEs at the maximum of 95th percentile ranges were below 80 for all population groups except for adolescents. The dietary exposures estimated using the maximum permitted levels would result in MOEs below 80 in all population groups at the maximum of the ranges of the mean, and for most of the population groups at both minimum and maximum of the ranges at the 95th percentile. The Panel concluded that this raises a safety concern for both dietary exposure scenarios. The Panel also performed a risk assessment for toxic elements present in sulfur dioxide–sulfites (E 220–228), based on data submitted by IBOs, and concluded that the maximum limits in the EU specifications for arsenic, lead and mercury should be lowered and a maximum limit for cadmium should be introduced.

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Memantine ameliorates learning and memory disturbance and the behavioral and psychological symptoms of dementia in thiamine-deficient mice

Cited by 6 publications

References 46 publications

Identification of Faecalibacterium prausnitzii strains for gut microbiome-based intervention in Alzheimer’s-type dementia

Identification of Faecalibacterium prausnitzii strains for gut microbiome-based intervention in Alzheimer’s-type dementia

Thiamine Deficiency Causes Long-Lasting Neurobehavioral Deficits in Mice

Follow‐up of the re‐evaluation of sulfur dioxide (E 220), sodium sulfite (E 221), sodium bisulfite (E 222), sodium metabisulfite (E 223), potassium metabisulfite (E 224), calcium sulfite (E 226), calcium bisulfite (E 227) and potassium bisulfite (E 228)

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