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Substantial synaptic dysfunction is detected in the early stages of AD when the hippocampus-dependent memory deficit becomes clinically detectable.
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Recognition memory was frequently weak at baseline, with deficits in verbal (7/12 < 5th percentile) and visual memory (8/12 < 5th percentile); over the period of follow-up, visual <span class="lh">memory deficits became more frequent (10/12 < 5th percentile).
Not surprisingly, working memory deficits have become a major therapeutic target for pharmacological and behavioral treatment strategies.
These data are in agreement with other studies showing that contextual fear memory is early affected in APP transgenic mouse models, whereas spatial and reference memory deficits only become apparent after 6 8 months [ 16, 34, 35].
A 7-3 Carolina deficit became a 27-7 halftimedgegedge
As cognitive and memory deficits progress, speech and language deficits become more evident and disabling (Groves-Wright et al 2004).
The working memory deficit in schizophrenia, first reported in the early 90s [1] has become an important cornerstone in understanding the pathophysiology of this disorder.
The treatment mitigated the epilepsy but also left him with a profound memory deficit.
Among them the hippocampal dependent memory deficit is well known.
Experimental CACPR caused hippocampal neuronal damage, microglial activation, and memory deficit in mice.
Integrin β2−/− mice also showed a remote memory deficit.
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