This suggested that visual memory fitted a more specific disease precursor model than verbal memory, a finding compatible with Skelley et al's study [5] showing that visual memory impairments were present in schizophrenic patients but absent in their non-affected adult relatives.
However, spatial memory impairments are present following both increases and decreases in hippocampal ACh (Bunce et al., 2004; Elvander et al., 2004), suggesting that ACh disruption may be the key factor, rather than ACh depletion per se.
Memory impairment was present at the onset in 15 patients, with word finding difficulties and stereotyped speech also being common.
These criteria do not require the traditional stepwise progression of cognitive impairment associated with multi-infarct dementia, and they are not conditional on memory impairment being present.
Thus, in schizophrenia, memory impairment is present at, or before, the first episode (i.e., by early adulthood; Mesholam-Gately and Giuliano 2009), whereas it only emerged here in older mice.
One should note that memory impairment, although present in most people with dementia, is not an essential requirement; rather, at least two cognitive domains must be impaired, and of course the other criteria must be met.
The proband (IV:23) presented with memory impairments and was given a final clinical diagnosis of FTD.
The AD model group presented with spatial learning and memory impairments.
Heterozygous R406W usually presents with clinical AD, with memory impairments related to hippocampal degeneration as seen in other MAPT mutations.
The aim of the present work was to assess early occurrence of working memory impairments in APP751SL mice.
