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This study was aimed at investigating the basic mechanisms of the normal repetition priming evoked by text re-reading procedures in Alzheimer's disease (AD) patients (Monti, Gabrieli, Wilson, & Reminger, 1994; Monti et al., 1997). For this purpose, we contrasted the reading facilitation elicited by previous reading or listening to a text in a sample of AD patients and a group of age-matched normal controls. Consistent with previous evidence in normal undergraduates (Levy & Kirsner, 1989), previous listening to a text decreased the successive reading time of the same text (cross-modality priming). However, the reading facilitation elicited by previous reading of the same text (within-modality priming) was significantly larger than the facilitation evoked by previous listening. Compared to normal controls, AD patients showed intact cross-modality and within-modality priming. These data are discussed in the light of alternative hypotheses regarding the basic mechanisms of impaired and spared repetition priming in degenerative demented patients.

In this study we compared memory performances of 29 probable patients with AD (17 mildly and 12 moderately demented) with those of 39 healthy young subjects, 36 elderly subjects (matched with the AD group for age and years of schooling), and 19 healthy very old subjects. In most of the memory tasks used in the present study, a progressive decline in performance was observed passing from the Young to the Elderly to the Very Old to the AD group. However, patients with AD were selectively impaired in the backward reproduction of verbal and spatial span sequences and in the semantic encoding of verbal material. These data are consistent with the hypothesis of not only quantitative but also a qualitative discontinuity between the process of normal aging and the dementia syndrome.

This study investigated the neural basis and cognitive mechanisms of disorders affecting the visual processing of human faces. Two patients affected by prosopagnosia (PA), 45 unilateral brain-damaged patients not previously selected for gnosic disturbance, and 52 normal subjects were administered three tasks involving visual matching of unfamiliar faces, identification of famous faces, and age attribution to unknown faces. Results confirmed that the right hemisphere (and particularly the posterior region) is critical for all of the main aspects of facial processing. Neuroradiological and PET examination in both PA patients revealed a lesion in the territory of the right posterior cerebral artery (infero-mesial areas of temporal and occipital lobes). Moreover, group comparisons showed that patients affected by a right posterior lesion obtained the worst scores on all tasks of our battery. Both group comparisons and single-case analyses pointed out that a deficient recognition of familiar faces is generally independent of perceptual disorders and, as such, should be considered mnestic in nature. Disorders in the age attribution, on the contrary, appear to be strictly associated with deficits in the perceptual analysis of unfamiliar faces.

The basic mechanisms of constructional apraxia (CA) are still a matter of debate. In this study we assessed the possible relationships between CA and performance on tasks assessing visual perception, low-level motor skill, manipulo-spatial ability, and general intellective efficiency in samples of healthy subjects, right-brain-damaged (RBD) and left-brain-damaged (LBD) patients. Multiple regression analyses, performed separately for the three groups, demonstrated that efficiency in perceiving the model as a whole is the factor mainly related to drawing performance of normal subjects. In the RBD group, instead, a disorder of the manipulo-spatial ability seems to play the most important role in producing CA. As for the LBD group, the most relevant finding is that patients drawing with the left hand are significantly more impaired than patients using the right hand and than control subjects. These results are discussed in relation to various hypotheses so far advanced to account for basic mechanisms of CA in unilateral brain-damaged patients.