The latter pathway, the nasal route, provides a direct passageway to the temporal lobe.

The only other cortical GM reduced in our sample was NAA and NAA/Cr in the right occipital region. Cre is present in all cells and is considered to be a marker of energy metabolism. The 1H-MR observed total-Cre signal Selleckchem Fostamatinib at 3T has contributions from both Cre and phosphocreatine. The phosphocreatine-Cre shuttle (a cellular energy transport system) is known to keep the MR-observed Cre signal stable in the brain of normal subjects. Previous MRS studies in the brain of normal humans[24] reported an increase of Cre concentration with increasing age, which was attributed to increased glial cell proliferation with aging. Furthermore, increased Cre found in brain pathologies (eg, multiple sclerosis and bipolar depression) was associated with either reactive gliosis[25] or hyper energy metabolism.[26] Therefore,

the increased Cre observed in our patient population might indicate either neuronal Rapamycin cost degeneration with concomitant increase in glial cell number or greater neuronal energy expenditure. It is not possible to ascertain which one of the mechanisms could be contributing to the increased Cre with the available MRS data in this study. Further studies are needed either to quantify myoinositol (a marker of gliosis) to rule out gliosis as the reason for the

observed increase in Cre or to quantify phosphocreatine and ATP by performing 31P MRS to assess changes in cellular energy metabolism.[25] The MRSI data acquired in this study at 70 ms echo time do not show quantifiable MR signals from myoinositol (See the spectra in Fig 1, at about 3.6 ppm). The significant reductions in metabolite ratios may also be due to increased Cre, as opposed medchemexpress to decreases in other metabolites. Few studies have examined the relationship between cognition and MRS-observed metabolites in PD. In this study, three significant correlations emerged; however, interpretation is limited by the lack of a meaningful pattern and the small sample size. From a descriptive viewpoint, 25% or more of PD patients performed below expectancy on naming, semantic fluency, visuospatial judgment, sustained attention, and card sorting and there is research showing activation of temporal lobe structures, the region with altered metabolites in our study, while performing many of these tasks.[27-29] An unexpected finding was the lack of impairment in verbal learning and memory performance, given the well-described role of the temporal lobes in memory. The fact that our memory testing was limited to free recall and subjects were not demented may explain the unimpaired memory performance.