In 13 - month old transgenic rats with advanced amyloid pathology we revealed marked contextual
fear conditioning deficits in homozygote animals.
Therefore,
fear conditioning deficits were detectable at early stages of the amyloid pathology, in the absence of amyloid plaques.
In our study, we observed strong Aβ - immunoreactivity in the amygdala at pre-plaque (intraneuronal) and post-plaque stages; changes which likely account for
the fear conditioning deficits reported at both time points.
Note the progression of auditory and contextual
fear conditioning deficits as the amyloid pathology advanced from pre - to post-plaque stages.
Not exact matches
In the
fear conditioning paradigm, only the combination of J147 and donepezil rescued the hippocampal - dependent
deficit in contextual and cued
fear conditioning, suggesting the compounds» synergistic effect for this particular type of memory (Figure 4C, D).
Furthermore, neuroimaging studies investigating the neural correlates that underlie emotional processing
deficits characteristic for youth with ODD problems, such as poor
fear conditioning and impaired processing of emotional faces (Glenn and Raine, 2008; Hyde et al., 2013; Blair et al., 2014; Baker et al., 2015), have suggested divergent results.
Furthermore, people with high levels of CU traits (psychopathic personality) have been shown to have three specific cognitive and emotional
deficits; a poor
conditioned fear response, reduced ability to recognise
fear, and
deficits in stimulus - reinforcement tasks (see Moul et al. [12] for a review).