CanCog Technologies Inc.

Toronto, Canada

CanCog Technologies Inc.

Toronto, Canada

Time filter

Source Type

Araujo J.A.,University of Toronto | Araujo J.A.,CanCog Technologies Inc. | Araujo J.A.,Kagera Inc | Greig N.H.,U.S. National Institute on Aging | And 6 more authors.
Journal of Alzheimer's Disease | Year: 2011

Similar to patients with Alzheimer's disease (AD), dogs exhibit age-dependent cognitive decline, amyloid-β (Aβ) pathology, and evidence of cholinergic hypofunction. The present study sought to further investigate the role of cholinergic hypofunction in the canine model by examining the effect of the cholinesterase inhibitors phenserine and donepezil on performance of two tasks, a delayed non-matching-to-position task (DNMP) designed to assess working memory, and an oddity discrimination learning task designed to assess complex learning, in aged dogs. Phenserine (0.5 mg/kg; PO) significantly improved performance on the DNMP at the longest delay compared to wash-out and partially attenuated scopolamine-induced deficits (15 μg/kg; SC). Phenserine also improved learning on a difficult version of an oddity discrimination task compared to placebo, but had no effect on an easier version. We also examined the effects of three doses of donepezil (0.75, 1.5, and 6 mg/kg; PO) on performance of the DNMP. Similar to the results with phenserine, 1.5 mg/kg of donepezil improved performance at the longest delay compared to baseline and wash-out, indicative of memory enhancement. These results further extend the findings of cholinergic hypofunction in aged dogs and provide pharmacological validation of the canine model with a cholinesterase inhibitor approved for use in AD. Collectively, these studies support utilizing the aged dog in future screening of therapeutics for AD, as well as for investigating the links among cholinergic function, Aβ pathology, and cognitive decline. © 2011-IOS Press and the authors. All rights reserved.


Araujo J.A.,University of Toronto | Araujo J.A.,CanCog Technologies Inc. | Nobrega J.N.,University of Toronto | Nobrega J.N.,Neuroimaging Research Section | And 4 more authors.
Pharmacology Biochemistry and Behavior | Year: 2011

Memory deficits associated with aging and Alzheimers disease have been linked to cholinergic dysfunction. The present study investigated this hypothesis by comparing the effects of the muscarinic cholinergic receptor antagonist scopolamine on recent memory performance and by examining muscarinic receptor density in aged and young dogs. Scopolamine (15 μg/kg; SC) was administered prior to testing young (M = 2.8 years) and aged (M = 13.0 years) dogs on a delayed-non-matching-to-position task (DNMP). Scopolamine significantly impaired performance of aged, but not young dogs. Muscarinic receptor density was assessed autoradiographically using the non-selective radioligand [3H]quinuclidinylbenzilate. Aged dogs (M = 14.1 years) showed significantly decreased density of muscarinic receptors in all brain regions examined except the cerebellum compared to young dogs (M = 3.7 years). The results are consistent with those seen in aged humans and Alzheimers patients and support the hypothesis of age-dependent cholinergic dysfunction in the dog, although this was not directly determined in the current study. These findings demonstrate that markers of cholinergic hypofunction, in addition to the natural cognitive decline and amyloid pathology previously noted, are seen in canine aging. Collectively, this supports the use of the aged dog as a model for examining early pathological events in the development of Alzheimers disease. © 2011 Elsevier Inc. All rights reserved.


Snigdha S.,University of California at Irvine | Milgram N.W.,CanCog Technologies Inc | Willis S.L.,University of Washington | Albert M.,Johns Hopkins University | And 3 more authors.
Neurobiology of Aging | Year: 2013

A major goal of animal research is to identify interventions that can promote successful aging and delay or reverse age-related cognitive decline in humans. Recent advances in standardizing cognitive assessment tools for humans have the potential to bring preclinical work closer to human research in aging and Alzheimer's disease. The National Institute of Health (NIH) has led an initiative to develop a comprehensive Toolbox for Neurologic Behavioral Function (NIH Toolbox) to evaluate cognitive, motor, sensory and emotional function for use in epidemiologic and clinical studies spanning 3 to 85 years of age. This paper aims to analyze the strengths and limitations of animal behavioral tests that can be used to parallel those in the NIH Toolbox. We conclude that there are several paradigms available to define a preclinical battery that parallels the NIH Toolbox. We also suggest areas in which new tests may benefit the development of a comprehensive preclinical test battery for assessment of cognitive function in animal models of aging and Alzheimer's disease. © 2013 Elsevier Inc.


Mongillo P.,University of Padua | Araujo J.A.,InterVivo Solutions Inc | Araujo J.A.,CanCog Technologies Inc | Araujo J.A.,University of Toronto | And 6 more authors.
Age | Year: 2013

Aged dogs spontaneously develop progressive decline in both cognitive and behavioral function, in addition to neuropathological changes, that collectively parallel several aspects of human aging and Alzheimer's disease progression and likely contribute to the development of canine cognitive dysfunction syndrome. In the current study, ethologically relevant spatial learning, retention, and reversal learning tasks were conducted, with the goal of expanding canine neuropsychological testing to pet dogs. Initially, dogs (N=44, aged 7.8±2.8 years, mean±SD) had to learn which of two alternative routes successfully led out of a T-maze. Two weeks later, long-term memory retention was assessed, immediately followed by a reversal learning task in which the previously correct route out of the maze was reversed compared with the initial learning and memory retention tasks. No effects of age were evident on the learning or retention tasks. However, older (≥8 years) dogs were significantly impaired on the reversal learning task compared with younger ones (<8 years). Moreover, trial response latency was significantly increased in aged dogs across both the initial and reversal learning tasks but not on the retention task, which suggests that processing speed was impaired by increasing age during the acquisition of novel spatial information but not during performance of previously learned responses. Overall, the current study provides a framework for assessing cognitive function in pet dogs, which should improve understanding of the effects of aging on cognition in the dog population. © American Aging Association 2013.


Creed M.C.,King's College | Milgram N.W.,King's College | Milgram N.W.,CanCog Technologies Inc.
Age | Year: 2010

Alzheimer's disease (AD) is the most prevalent form of dementia, affecting an estimated 4.8 million people in North America. For the past decade, the amyloid cascade hypothesis has dominated the field of AD research. This theory posits that the deposition of amyloid-beta protein (Aβ) in the brain is the key pathologic event in AD, which induces a series of neuropathological changes that manifest as cognitive decline and eventual dementia. Based on this theory, interventions that reduce Aβ burden in the brain would be expected to alleviate both the neuropathological changes and dementia, which characterize AD. Several diverse pharmacological strategies have been developed to accomplish this. These include inhibiting the formation of Aβ, preventing the aggregation of Aβ into insoluble aggregates, preventing the entry of Aβ into the brain from the periphery and enhancing the clearance of Aβ from the central nervous system. To date, no amyloid-modifying therapy has yet been successful in phase 3 clinical trials; however, several trials are currently underway. This article provides a review of the status of amyloid-modifying therapies and the implications for the amyloid cascade hypothesis. © 2010 American Aging Association, Media.


Snigdha S.,University of California at Irvine | de Rivera C.,CanCog Technologies Inc. | Milgram N.W.,CanCog Technologies Inc. | Cotman C.W.,University of California at Irvine
Frontiers in Aging Neuroscience | Year: 2014

Exercise has been shown to reduce age-related losses in cognitive function including learning and memory, but the mechanisms underlying this effect remain poorly understood. Memory formation occurs in stages that include an initial acquisition phase, an intermediate labile phase, and then a process of consolidation which leads to long-term memory formation. An effective way to examine the mechanism by which exercise improves memory is to introduce the intervention (exercise), post-acquisition, making it possible to selectively examine memory storage and consolidation. Accordingly we evaluated the effects of post-trial exercise (10 min on a treadmill) on memory consolidation in aged canines both right after, an hour after, and 24 h after acute exercise training in concurrent discrimination, object location memory (OLM), and novel object recognition tasks. Our study shows that post-trial exercise facilitates memory function by improving memory consolidation in aged animals in a time-dependent manner. The improvements were significant at 24 h post-exercise and not right after or 1 h after exercise. Aged animals were also tested following chronic exercise (10 min/day for 14 consecutive days) on OLM or till criterion were reached (for reversal learning task). We found improvements from a chronic exercise design in both the object location and reversal learning tasks. Our studies suggest that mechanisms to improve overall consolidation and cognitive function remain accessible even with progressing age and can be re-engaged by both acute and chronic exercise. © 2014 Snigdha, de Rivera, Milgram and Cotman.


Snigdha S.,University of California at Irvine | de Rivera C.,CanCog Technologies Inc. | Milgram N.W.,CanCog Technologies Inc. | Cotman C.W.,University of California at Irvine
Neurobiology of aging | Year: 2016

A growing body of research has focused on modifiable risk factors for prevention and attenuation of cognitive decline in aging. This has led to an unprecedented interest in the relationship between diet and cognitive function. Several preclinical and epidemiologic studies suggest that dietary intervention can be used to improve cognitive function but randomized controlled trials are increasingly failing to replicate these findings. Here, we use a canine model of aging to evaluate the effects of specific components of diet supplementation which contain both antioxidants and a combination of mitochondrial cofactors (lipoic acid [LA] and acetyl-l-carnitine) on a battery of cognitive functions. Our data suggest that supplementation with mitochondrial cofactors, but not LA or antioxidant alone, selectively improve long-term recall in aged canines. Furthermore, we found evidence that LA alone could have cognitive impairing effects. These results contrast to those of a previous longitudinal study in aged canine. Our data demonstrate that one reason for this difference may be the nutritional status of animals at baseline for the 2 studies. Overall, this study suggests that social, cognitive, and physical activity together with optimal dietary intake (rather than diet alone) promotes successful brain aging. Published by Elsevier Inc.


Patent
Cancog Technologies Inc. | Date: 2013-09-25

A system and method for cognitive enrichment of an animal. At least one display device is configured to display stimuli to an animal. At least one input device is configured to accept input from the animal. At least one reward dispenser is configured to dispense a reward to the animal. At least one processor is communicatively coupled with the at least one display device, the at least one input device, and the at least one reward dispenser. Execution of computer-readable instructions causes the at least one processor to carry out steps including displaying one or more stimuli to the animal using the at least one display device, accepting an input from the animal corresponding to at least one of the one or more stimuli, making a dispensing decision based on the input, and dispensing a reward using the at least one reward dispenser based on the dispensing decision.


Patent
CanCog Technologies Inc. | Date: 2012-09-12

An apparatus and method for cognitive assessment and training of an animal subject. A subject is placed in a testing environment, such as a subject chamber of a cognitive assessment and training apparatus. At least one cognitive assessment and training session comprising a plurality of trials is performed. In a trial, a trial assembly is prepared at a first level. The trial assembly includes at least one stimuli and a reward, where a target stimuli of the at least one stimuli is associated with the reward. The subject is allowed access to the stimuli. When a correct response is determined from the subject, the subject is allowed to access a reward associated with the correct response. The subject is advanced to trials at a next level when a learning criterion is reached. At least one cognitive assessment score is generated based on the plurality of trials and the at least one cognitive assessment and training session.


Patent
CanCog Technologies Inc. | Date: 2014-06-10

A system and method for cognitive enrichment of an animal. At least one display device is configured to display stimuli to an animal. At least one input device is configured to accept input from the animal. At least one reward dispenser is configured to dispense a reward to the animal. At least one processor is communicatively coupled with the at least one display device, the at least one input device, and the at least one reward dispenser. Execution of computer-readable instructions causes the at least one processor to carry out steps including displaying one or more stimuli to the animal using the at least one display device, accepting an input from the animal corresponding to at least one of the one or more stimuli, making a dispensing decision based on the input, and dispensing a reward using the at least one reward dispenser based on the dispensing decision.

Loading CanCog Technologies Inc. collaborators
Loading CanCog Technologies Inc. collaborators