The hippocampus is crucial for conscious, explicit memory, but whether it is also involved in nonconscious, implicit memory is uncertain. We investigated with functional magnetic resonance imaging whether implicit learning engages the hippocampus and interacts with subsequent explicit learning. The presentation of subliminal faces-written profession pairs for implicit learning was followed by the explicit learning of supraliminal pairs composed of the same faces combined with written professions semantically incongruous to those presented subliminally (experiment 1), semantically congruous professions (experiment 2), or identical professions (experiment 3). We found that implicit face-profession learning interacted with explicit face-profession learning in all experiments, impairing the explicit retrieval of the associations. Hippocampal activity increased during the subliminal presentation of face-profession pairs versus face-nonword pairs and correlated with the later impairment of explicit retrieval. These findings suggest that implicit semantic associative learning engages the hippocampus and influences explicit memory.

We studied the role of the hippocampus in memory retrieval at 1 day and 1 month following associative learning of word pairs. Retrieval-related brain activity was recorded using functional magnetic resonance imaging in 20 healthy students, of which 12 were good learners and eight were poor learners. At the day lag, the poor learners exhibited enhanced neural recruitment in the hippocampus and neocortex to reach a retrieval performance comparable to that of the good learners. Over the 20 subjects, there was a positive correlation between retrieval-related hippocampal activity at the day lag and forgetting over the month retention interval (the greater the activity, the more forgetting). Although the poor learners' retrieval performance declined dramatically from the day to the month lag, the good learners maintained a high retrieval performance, which distinguishes them as good memory consolidators. Their retrieval-related hippocampal and neocortical activity increased from the day to the month lag. This increase was observed both when retrieval performance was matched between the day and the month lag and when the learning procedure for information retrieved at the day and the month lag was matched. This activity increase in the task-specialized neural network from the day lag to the month lag may reflect an increase in task demands or the proliferation of hippocampal-neocortical memory traces during memory consolidation as suggested by the multiple trace theory.

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Tissue inhibitor of metalloproteinases 1 (TIMP-1) inhibits several proteinases including a disintegrin and metalloproteinase 10 (ADAM10), a major alpha-secretase that cleaves the beta-amyloid precursor protein within its amyloidogenic Abeta domain. The gene encoding TIMP-1 (TIMP 1) maps to the short arm of the X chromosome, in a region previously suggested as conferring genetic susceptibility for Alzheimer's disease (AD). To determine whether genetic variability of TIMP 1 contributes to the pathogenesis of AD, we analysed one single nucleotide polymorphism within TIMP 1 and one single nucleotide polymorphism in the 5'-untranslated region of TIMP 1 in patients with AD and control subjects from two independent and ethnically different populations. We did not observe any association between TIMP 1 genotypes and the diagnosis of AD in men or women. We also measured TIMP-1 protein levels in the cerebrospinal fluid of patients with AD, healthy control subjects, and patients with other neurological disorders. TIMP-1 levels were similar in all groups. In addition, no significant differences were observed after stratification for TIMP 1 genotypes. Our data show that neither genetic variability nor protein levels of TIMP-1 are associated with AD.

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