Learning ability in aged beagle dogs is preserved by behavioral enrichment and dietary fortification: a two-year longitudinal study

Milgram, Norton W.; Head, Elizabeth; Zicker, Steven C.; Ikeda-Douglas, Candace J; Murphey, Heather; Muggenburg, Bruce A.; Siwak, Christina T.; Tapp, Dwight; Cotman, Carl W.

doi:10.1016/j.neurobiolaging.2004.02.014

Cited by 171 publications

(128 citation statements)

References 45 publications

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“…Discrimination learning was significantly improved by behavioral enrichment. Reversal learning was improved by both behavioral enrichment and mixture feeding [91]. Oxidative stress biomarkers, i.e.…”

Section: Antioxidant Defensementioning

confidence: 97%

The Effects and Mechanisms of Mitochondrial Nutrient α-Lipoic Acid on Improving Age-Associated Mitochondrial and Cognitive Dysfunction: An Overview

2007

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We have identified a group of nutrients that can directly or indirectly protect mitochondria from oxidative damage and improve mitochondrial function and named them "mitochondrial nutrients". The direct protection includes preventing the generation of oxidants, scavenging free radicals or inhibiting oxidant reactivity, and elevating cofactors of defective mitochondrial enzymes with increased Michaelis-Menten constant to stimulate enzyme activity, and also protect enzymes from further oxidation, and the indirect protection includes repairing oxidative damage by enhancing antioxidant defense systems either through activation of phase 2 enzymes or through increase in mitochondrial biogenesis. In this review, we take alpha-lipoic acid (LA) as an example of mitochondrial nutrients by summarizing the protective effects and possible mechanisms of LA and its derivatives on age-associated cognitive and mitochondrial dysfunction of the brain. LA and its derivatives improve the age-associated decline of memory, improve mitochondrial structure and function, inhibit the age-associated increase of oxidative damage, elevate the levels of antioxidants, and restore the activity of key enzymes. In addition, co-administration of LA with other mitochondrial nutrients, such as acetyl-L: -carnitine and coenzyme Q10, appears more effective in improving cognitive dysfunction and reducing oxidative mitochondrial dysfunction. Therefore, administrating mitochondrial nutrients, such as LA and its derivatives in combination with other mitochondrial nutrients to aged people and patients suffering from neurodegenerative diseases, may be an effective strategy for improving mitochondrial and cognitive dysfunction.

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Section: Antioxidant Defensementioning

confidence: 97%

The Effects and Mechanisms of Mitochondrial Nutrient α-Lipoic Acid on Improving Age-Associated Mitochondrial and Cognitive Dysfunction: An Overview

2007

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“…41,43 For example, feeding a diet enriched in antioxidants, L-carnitine, and omega-3 fatty acids plus providing environmental enrichment resulted in significant improvements in learning and memory in older dogs. 44,45 Medium-chain triglycerides are also proved to enhance brain function in dogs and humans. 46 A recent study in middle-aged and older cats found a combination of fish oil, antioxidants, arginine, and key B vitamins successfully enhanced brain functions.…”

Section: Therapeutic Nutrition For Specific Conditions Feline Cognitimentioning

confidence: 99%

Nutrition of Aging Cats

Laflamme¹,

Gunn-Moore

2014

Veterinary Clinics of North America: Small Animal Practice

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“…Also, smaller studies with more intensive training have reported some modest improvement of cognitive function not directly related to the learned task [75]. In the aged canine model of AD, which is closer to sporadic AD than transgenic mouse models, environmental enrichment caused a significant improvement in cognitive performance, but Aβ-vaccination did not [76–78]. Interestingly, both strategies reduced Aβ load, but this was not strongly correlated with cognitive performance.…”

Section: Therapeutic Implicationsmentioning

confidence: 99%

Homeostatic Disinhibition in the Aging Brain and Alzheimer's Disease

Gleichmann

Chow

Mattson

2011

JAD

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In this article we propose that impaired efficiency of glutamatergic synaptic transmission and a compensatory reduction in inhibitory neurotransmission, a process called homeostatic dishinhibition, occurs in the aging brain and more dramatically in Alzheimer’s disease (AD). Homeostatic disinhibition may help understand certain features of the aging brain and AD including: 1) the increased risk for epileptic seizures, especially in the early phase of the disease; 2) the reduced ability to generate γ-oscillations and 3) the increase in neuronal activity as measured by functional MRI. Homeostatic disinhibition may be the major mechanism that activates cognitive reserve. Modulating neuronal activity may therefore be a viable therapeutic strategy in AD that can complement existing anti-amyloid strategies. Specifically, enhancing endogenous glutamatergic synaptic transmission through increased co-agonist signaling or through positive allosteric modulation of metabotropic glutamatergic receptors appears as an attractive strategy. Alternatively, further reduction of GABAergic signaling may work as well, although care has to be taken to prevent epileptic seizures.

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Learning ability in aged beagle dogs is preserved by behavioral enrichment and dietary fortification: a two-year longitudinal study

Cited by 171 publications

References 45 publications

The Effects and Mechanisms of Mitochondrial Nutrient α-Lipoic Acid on Improving Age-Associated Mitochondrial and Cognitive Dysfunction: An Overview

The Effects and Mechanisms of Mitochondrial Nutrient α-Lipoic Acid on Improving Age-Associated Mitochondrial and Cognitive Dysfunction: An Overview

Nutrition of Aging Cats

Homeostatic Disinhibition in the Aging Brain and Alzheimer's Disease

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