Alzheimer's disease pattern of brain atrophy predicts cognitive decline in Parkinson's disease.

Research suggests overlap in brain regions undergoing neurodegeneration in Parkinson's and Alzheimer's disease. To assess the clinical significance of this, we applied a validated Alzheimer's disease-spatial pattern of brain atrophy to patients with Parkinson's disease with a range of cognitive abilities to determine its association with cognitive performance and decline. At baseline, 84 subjects received structural magnetic resonance imaging brain scans and completed the Dementia Rating Scale-2, and new robust and expanded Dementia Rating Scale-2 norms were applied to cognitively classify participants. Fifty-nine non-demented subjects were assessed annually with the Dementia Rating Scale-2 for two additional years. Magnetic resonance imaging scans were quantified using both a region of interest approach and voxel-based morphometry analysis, and a method for quantifying the presence of an Alzheimer's disease spatial pattern of brain atrophy was applied to each scan. In multivariate models, higher Alzheimer's disease pattern of atrophy score was associated with worse global cognitive performance (ß = -0.31, P = 0.007), including in non-demented patients (ß = -0.28, P = 0.05). In linear mixed model analyses, higher baseline Alzheimer's disease pattern of atrophy score predicted long-term global cognitive decline in non-demented patients [F(1, 110) = 9.72, P = 0.002], remarkably even in those with normal cognition at baseline [F(1, 80) = 4.71, P = 0.03]. In contrast, in cross-sectional and longitudinal analyses there was no association between region of interest brain volumes and cognitive performance in patients with Parkinson's disease with normal cognition. These findings support involvement of the hippocampus and parietal-temporal cortex with cognitive impairment and long-term decline in Parkinson's disease. In addition, an Alzheimer's disease pattern of brain atrophy may be a preclinical biomarker of cognitive decline in Parkinson's disease.

Neural changes following remediation in adult developmental dyslexia.

Brain imaging studies have explored the neural mechanisms of recovery in adults following acquired disorders and, more recently, childhood developmental disorders. However, the neural systems underlying adult rehabilitation of neurobiologically based learning disabilities remain unexplored, despite their high incidence. Here we characterize the differences in brain activity during a phonological manipulation task before and after a behavioral intervention in adults with developmental dyslexia. Phonologically targeted training resulted in performance improvements in tutored compared to nontutored dyslexics, and these gains were associated with signal increases in bilateral parietal and right perisylvian cortices. Our findings demonstrate that behavioral changes in tutored dyslexic adults are associated with (1) increased activity in those left-hemisphere regions engaged by normal readers and (2) compensatory activity in the right perisylvian cortex. Hence, behavioral plasticity in adult developmental dyslexia involves two distinct neural mechanisms, each of which has previously been observed either for remediation of developmental or acquired reading disorders.

Phonological decoding involves left posterior fusiform gyrus.

Aloud reading of novel words is achieved by phonological decoding, a process in which grapheme-to-phoneme conversion rules are applied to "sound out" a word's spoken representation. Numerous brain imaging studies have examined the neural bases of phonological decoding by contrasting pseudoword (pronounceable nonwords) to real word reading. However, only a few investigations have examined pseudoword reading under both aloud and silent conditions, task parameters that are likely to significantly alter the functional anatomy of phonological decoding. Subjects participated in an fMRI study of aloud pseudoword, aloud real word, silent pseudoword, and silent real word reading. Using this two-by-two design, we examined effects of word-type (real words vs. pseudowords) and response-modality (silent vs. aloud) and their interactions. We found 1) four regions to be invariantly active across the four reading conditions: the anterior aspect of the left precentral gyrus (Brodmann's Area (BA) 6), and three areas within the left ventral occipitotemporal cortex; 2) a main effect of word-type (pseudowords > words) in left inferior frontal gyrus and left intraparietal sulcus; 3) a main effect of response-modality (aloud > silent) that included bilateral motor, auditory, and extrastriate cortex; and 4) a single left hemisphere extrastriate region showing a word-type by response-modality interaction effect. This region, within the posterior fusiform cortex at BA 19, was uniquely modulated by varying phonological processing demands. This result suggests that when reading, word forms are subject to phonological analysis at the point they are first recognized as alphabetic stimuli and BA 19 is involved in processing the phonological properties of words.