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The disruption of BBB in small vessel disease has been documented using dynamic contrast-enhanced http://www.selleckchem.com/products/DAPT-GSI-IX.html magnetic resonance imaging in live patients and through immunohistochemistry of immunoglobulins and fibrinogen of brain tissue [33]?and?[34]. Cortical hypometabolism and hypoperfusion have been detected with functional imaging like positron emission tomography in patients of VaD in comparison with healthy controls [35] and by two-dimensional xenon-133 inhalation technique in the ipsilateral fronto-parietal cortex in the presence of sub-cortical infarcts [36]. Considering chronic leakage of fluid and macromolecules, a likely consequence will be induction of an inflammatory response in the temporal cortex of VaD brain. Subsequently, curating the proteomic data set for other hallmarks of inflammation identified few adhesion molecules (e.g. L1CAM, NCAM1, ICAM5) showing an up-regulation in the VaD group (Table?2, Figs.?3, 4). The decrease in HSPA4, which normally functions as a chaperone and protects cells from inflammation during cerebral ischemic injury, may further worsen the inflammatory condition?[37]. The levels of L1CAM and NCAM were found to be higher in the cerebrospinal fluid (CSF) of VaD, AD and MIX dementia patients compared to non-demented controls [38]. Soluble form of ICAM5 has been detected in the serum within the first 48?h of cerebral hypoxic�Cischemic injury of mice, where shredded neuronal ICAM5 could act as an anti-inflammatory agent by suppressing the T-cell activation [39]?and?[40]. In the human brain, iron is ubiquitous and is selleck chemicals responsible for the activity of key enzymes (e.g. cytochromes, mitochondrial non-haem iron proteins) and for the synthesis of neurotransmitters. Most of the total iron in a healthy brain is sequestered by ferritin Tolmetin thus limiting its pro-oxidant potential. Brain ferritin-associated iron levels increase with age. Abnormal elevation of brain iron and ferritin has been reported in the neurodegenerative dementias (i.e. AD, PD and dementia with Lewy Bodies) suggesting that increased iron levels may contribute to the misfolding and subsequent deposition of key proteins [41]. Although consistent correlation between iron accumulation and cognitive dysfunction has been documented in animal or clinical studies related to neurodegenerative diseases like AD, similar reports are scarce in the area of VaD [42]. Here, we report an increase of brain ferritin (H- and L-isoforms) levels of VaD patients compared to the age-matched control group (Table?2, Fig.?3). Interestingly, out of the tested fourteen candidates for validation, only the levels of ferritin (r?=?0.76, p?