Using animal models to address the memory deficits of Wernicke-Korsakoff syndrome.

2001 ◽  
pp. 281-292 ◽  
Author(s):  
Angela K. Hochhalter ◽  
Whitney A. Sweeney ◽  
Lisa M. Savage ◽  
Bruce L. Bakke ◽  
J. Bruce Overmier
Keyword(s):  
Animal Models ◽  
Memory Deficits ◽  
Korsakoff Syndrome

scholarly journals Disinhibited-Like Behavior Correlates With Frontal Cortex Damage in Alcohol-Induced Wernicke-Korsakoff Syndrome

2021 ◽  
Author(s):  
Marta Moya ◽  
Leticia López-Valencia ◽  
Borja García-Bueno ◽  
Laura Orio
Keyword(s):  
Frontal Cortex ◽  
Nitrosative Stress ◽  
Inflammatory Responses ◽  
Cell Damage ◽  
Combined Treatment ◽  
Memory Deficits ◽  
Combined Treatments ◽  
Therapeutic Approaches ◽  
Korsakoff Syndrome ◽  
Disease Specific

Wernicke-Korsakoff syndrome (WKS) is induced by thiamine deficiency (TD) and mainly related to alcohol consumption. Frontal cortex dysfunction has been associated to impulsivity and disinhibition in WKS patients. The pathophysiology involves oxidative stress, excitotoxicity and inflammatory responses leading to neuronal death, but the relative contributions of each factor (alcohol and TD, isolate or in interaction) to these phenomena are still poorly understood. A rat model was used by forced consumption of 20% (w/v) alcohol for 9 months (CA), TD hit (TD diet + pyrithiamine 0.25 mg/kg, i.p. daily injections the last 12 days of experimentation; TDD), and both combined treatments (CA+TDD). Motor and cognitive performance and cortical damage were examined. CA caused hyperlocomotion as a possible sensitization of ethanol-induced excitatory effects and recognition memory deficits. In addition, CA+TDD animals showed a disinhibited-like behavior, which appears to be dependent on TDD. Also, combined treatment led to more pronounced alterations in nitrosative stress, lipid peroxidation, apoptosis and cell damage markers. Correlations between injury signals and disinhibition suggest that CA+TDD disrupts behaviors dependent on the frontal cortex. Our study sheds light on the potential disease-specific mechanisms, reinforcing the need for neuroprotective therapeutic approaches along with preventive treatments for the nutritional deficiency in WKS.

scholarly journals Mild cognitive impairment: animal models

2004 ◽  
Vol 6 (4) ◽  
pp. 369-377 ◽  
Keyword(s):  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Animal Models ◽  
Cognitive Aging ◽  
Animal Species ◽  
Early Stage ◽  
Memory Deficits ◽  
Laboratory Animals ◽  
Transitional State ◽  
Rats And Mice

Mild cognitive impairment (MCI) is an aspect of cognitive aging that is considered to be a transitional state between normal aging and the dementia into which it may convert. Appropriate animal models are necessary in order to understand the pathogenic mechanisms of MCI and develop drugs for its treatment. In this review, we identify the features that should characterize an animal model of MCI, namely old age, subtle memory impairment, mild neuropathological changes, and changes in the cholinergic system, and the age at which these features can be detected in laboratory animals. These features should occur in aging animals with normal motor activity and feeding behavior. The animal models may be middle-aged rats and mice, rats with brain ischemia, transgenic mice overexpressing amyloid precursor protein and presenilin 1 (tested at an early stage), or aging monkeys. Memory deficits can be detected by selecting appropriately difficult behavioral tasks, and the deficits can be associated with neuropathological alterations. The reviewed literature demonstrates that, under certain conditions, these animal species can be considered to be MCI models, and that cognitive impairment in these models responds to drug treatment.

scholarly journals Reduced Smoothened level rescues Aβ-induced memory deficits and neuronal inflammation in animal models of Alzheimer's disease

2018 ◽  
Vol 45 (5) ◽  
pp. 237-246 ◽  
Author(s):  
Weiwei Ma ◽  
Mengnan Wu ◽  
Siyan Zhou ◽  
Ye Tao ◽  
Zuolei Xie ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Models ◽  
Memory Deficits

Herbal Treatments for ECS-Induced Memory Deficits: A Review of Research and a Discussion on Animal Models

2000 ◽  
Vol 16 (2) ◽  
pp. 144-156 ◽  
Author(s):  
Chittaranjan Andrade ◽  
S. Sudha ◽  
B. V. Venkataraman
Keyword(s):  
Animal Models ◽  
Memory Deficits

scholarly journals The newly synthesized linoleic acid derivative DCP-LA ameliorates memory deficits in animal models treated with amyloid-beta peptide and scopolamine

2005 ◽  
Vol 5 (4) ◽  
pp. 122-126 ◽  
Author(s):  
Tetsu NAGATA ◽  
Satoshi YAMAMOTO ◽  
Takahiro YAGUCHI ◽  
Hiroyuki ISO ◽  
Akito TANAKA ◽  
...  
Keyword(s):  
Linoleic Acid ◽  
Animal Models ◽  
Acid Derivative ◽  
Amyloid Beta ◽  
Memory Deficits ◽  
Amyloid Beta Peptide ◽  
Beta Peptide

Experimental Models for the Discovery of Novel Anticonvulsant Drugs: Focus on Pentylenetetrazole-Induced Seizures and Associated Memory Deficits

2020 ◽  
Vol 26 (15) ◽  
pp. 1693-1711 ◽  
Author(s):  
Alaa Alachkar ◽  
Shreesh K. Ojha ◽  
Adel Sadeq ◽  
Abdu Adem ◽  
Annika Frank ◽  
...  
Keyword(s):  
Animal Models ◽  
Neuronal Excitability ◽  
Memory Deficits ◽  
Experimental Models ◽  
In Vivo Studies ◽  
Anticonvulsant Effect ◽  
Myoclonic Seizure ◽  
Morphological Alterations ◽  
Seizure Models

: Epilepsy is a chronic neurological disorder characterized by irregular, excessive neuronal excitability, and recurrent seizures that affect millions of patients worldwide. Currently, accessible antiepileptic drugs (AEDs) do not adequately support all epilepsy patients, with around 30% patients not responding to the existing therapies. As lifelong epilepsy treatment is essential, the search for new and more effective AEDs with an enhanced safety profile is a significant therapeutic goal. Seizures are a combination of electrical and behavioral events that can induce biochemical, molecular, and anatomic changes. Therefore, appropriate animal models are required to evaluate novel potential AEDs. Among the large number of available animal models of seizures, the acute pentylenetetrazole (PTZ)-induced myoclonic seizure model is the most widely used model assessing the anticonvulsant effect of prospective AEDs, whereas chronic PTZ-kindled seizure models represent chronic models in which the repeated administration of PTZ at subconvulsive doses leads to the intensification of seizure activity or enhanced seizure susceptibility similar to that in human epilepsy. In this review, we summarized the memory deficits accompanying acute or chronic PTZ seizure models and how these deficits were evaluated applying several behavioral animal models. Furthermore, major advantages and limitations of the PTZ seizure models in the discovery of new AEDs were highlighted. With a focus on PTZ seizures, the major biochemicals, as well as morphological alterations and the modulated brain neurotransmitter levels associated with memory deficits have been illustrated. Moreover, numerous medicinal compounds with concurrent anticonvulsant, procognitive, antioxidant effects, modulating effects on several brain neurotransmitters in rodents, and several newly developed classes of compounds applying computer-aided drug design (CADD) have been under development as potential AEDs. The article details the in-silico approach following CADD, which can be utilized for generating libraries of novel compounds for AED discovery. Additionally, in vivo studies could be useful in demonstrating efficacy, safety, and novel mode of action of AEDs for further clinical development.

scholarly journals Interaction Between Emotion and Memory: Importance of Mammillary Bodies Damage in a Mouse Model of the Alcoholic Korsakoff Syndrome

2005 ◽  
Vol 12 (4) ◽  
pp. 275-287 ◽  
Author(s):  
Daniel Béracochéa
Keyword(s):  
Mouse Model ◽  
Episodic Memory ◽  
Memory Deficits ◽  
Brain Network ◽  
Mammillary Bodies ◽  
Retrieval Processes ◽  
Korsakoff Syndrome ◽  
Essential Components ◽  
Emotion And Memory ◽  
Fear Reactivity

Chronic alcohol consumption (CAC) can lead to the Korsakoff syndrome (KS), a memory deficiency attributed to diencephalie damage and/or to medial temporal or cortical related dysfunction. The etiology of KS remains unclear. Most animal models of KS involve thiaminedeficient diets associated with pyrithiamine treatment. Here we present a mouse model of CAC-induced KS. We demonstrate that CAC-generated retrieval memory deficits in working/ episodic memory tasks, together with a reduction of fear reactivity, result from damage to the mammillary bodies (MB). Experimental lesions of MB in non-alcoholic mice produced the same memory and emotional impairments. Drugs having anxiogenic-like properties counteract such impairments produced by CAC or by MB lesions. We suggest (a) that MB are the essential components of a brain network underlying emotional processes, which would be critically important in the retrieval processes involved in working/ episodic memory tasks, and (b) that failure to maintain emotional arousal due to MB damage can be a main factor of CAC-induced memory deficits. Overall, our animal model fits well with general neuropsychological and anatomic impairments observed in KS.

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