Diabetes is also associated with cognitive defect, including impaired performance in cognition and memory [ 10, 11].
This knowledge is essential to understand not only the molecular mechanisms of cognition but also the defects underlying the cognitive impairment that accompany most lipidosis.
This separation between cognitions and feelings, together with the view that feelings are defects that disturb cognitions, means that feelings are regarded as purely negative.
Clinical outcomes include depressed growth, diarrhea, impotence and delayed sexual maturation, alopecia, eye and skin lesions, impaired appetite, altered cognition, impaired host defense properties, defects in carbohydrate utilization, and reproductive teratogenesis.
Although high plasma levels of cholesterol in some instances correlate with an increased incidence of AD, there is no direct evidence that alterations in cholesterol homeostasis are responsible for the defects in memory and cognition.
Assessment of molecular defects that underlie cognitive deficits observed in mendelian disorders provides a unique opportunity to identify key regulators of human cognition.
The cerebellum plays a critical role in motor control, cognition, and social interaction, suggesting that cerebellar defects likely contribute to NF1-associated neurodevelopmental disorders.
These data indicate that the defects in synaptic transmission and cognition are not caused by a change in expression of key synaptic proteins.
Nonetheless, these mutations result in severe defects (for example, in movement, breathing, cognition, vision or suckling) that render the pups unviable.
Another reason why cognition is an important quality is that it is not necessarily a defect whereas the other qualities are always defects.
