In the brain after infarction or trauma, the tissue becomes pannecrotic and forms a cavity. In such situation, a scaffold is necessary to produce new tissue. In this study, we implanted a new porous gelatin-siloxane hybrid derived from gelatin and 3-(glycidoxypropyl) trimethoxysilane (gelatin-GPTMS) scaffolds into a brain defect, and investigated whether it makes a new brain tissue. In addition, vascular endothelial growth factor (VEGF) was added on gelatin- GPTMS scaffolds and its effect on tissue regeneration was examined. At 30 days after the implantation, the marginal territory of the scaffolds became occupied by newly formed tissue. Immunohistochemical analysis revealed that the new tissue was constituted by endothelial, astroglial and microglial cells, some of which were labeled for bromodeoxyuridine (BrdU). Addition of VEGF promoted numbers of these cells. Thus, combination of gelatin-GPTMS scaffolds and VEGF is preferable for brain regeneration. Keywords: Brain, scaffold, tissue regeneration, vascular endothelial growth factor
To examine comprehensive clinical evaluations of frontotemporal dementia (FTD) patients compared with Alzheimer's disease (AD) patients.We used eight batteries and the touch panel test to retrospectively analyze 41 FTD patients compared with 121 AD patients. Furthermore, 34 FTD and all 121 AD patients were evaluated with a frontotemporal dementia-Alzheimer's disease index (FA index), which we developed for novel diagnosis with magnetic resonance imaging.Frontal assessment battery, geriatric depression scale, and Abe's behavioral and psychological symptom of dementia score were significantly worse in FTD patients than in AD patients ( **p < 0.01 in FAB, **p < 0.01 in the geriatric depression scale, and ***p < 0.001 in Abe's behavioral and psychological symptom of dementia score), although there was no significant difference in the other five scores. The finding mistakes game score of the touch panel test was worse in FTD than in AD ( *p < 0.05). The receiver operating characteristic curve of the FA index showed 91.4% sensitivity and 89.3% specificity with the FA index ≤0.6015 to discriminate FTD from AD.Combining clinical scores, a computerized touch panel test, and the FA index will help to provide a more accurate diagnosis of FTD in contrast to AD.
We describe a case presenting with facial and hypoglossal nerve paresis due to cortical cerebral infarction. A 54-year-old man visited our hospital complaining of sudden episode of dysarthria and facial paresis. Neurological findings revealed tongue deviation to the left and left facial paresis with forehead wrinkling while neither limb paralysis nor sensory impairment was observed. Head CT performed on day 3 after onset revealed a cortical infarction in the right prefrontal gyrus. Symptoms gradually improved with medical management. This patient had isolated facial and hypoglossal nerve paresis without other neurological symptoms. Patients with mild paresis of cranial nerves should be diagnosed carefully, because their paresis could be supranuclear type.
The increase in the ratio of Aβ42 production has been widely accepted as pathological “gain of function” which determines the onset of familial AD pathology. However, it has not been studied whether the increase in the ratio of Aβ42 production plays a role in the pathological process of sporadic AD that occupies most of AD cases. Instead, many studies concerning an aspect of Aβ degradation/metabolism in sporadic AD have been conducted and indicated the importance of the Aβ degradation mechanism. To understand this trend, it is important to consider the highly aggregatable biochemical feature of Aβ42. Remarkably, in the CSF of sporadic AD patients, the Aβ42 level does not correspond to its generation in the brain. That is, insoluble Aβ42 levels are extremely high and soluble Aβ42 levels decrease in the sporadic AD brains. So far, there are no plans to address the level of Aβ42 production in sporadic AD brains without pathological mutations. Therefore, one of the most important issues remains unsolved. Cultured cells and Human CSF samples were used. Here, we indicated that the ratio of Aβ42 production increases in brains of sporadic AD patients bearing wt βAPP and presenilins as well as familial AD patients. This was made possible by our discovery of a novel peptide that is an elongated form of APLP1-derived Aβ-like peptide and is produced by the same process as Aβ42 but does not accumulate in the brain. We were able to make conclusions by using the level of the peptide in the CSF as a surrogate marker for Aβ42 in the brain of AD patients. First, this study addresses the pathogenesis of sporadic AD. Second, the discovery of this novel Aβ42 surrogate marker has clinical importance. Accumulation of Aβ42 is thought to begin long before onset of AD. If an increase in the relative Aβ42 production in the brain contributes to Aβ42 aggregation of sporadic AD patients, an elevated ratio of the elongated peptide in the CSF should precede accumulation of Aβ42 in the brain and should therefore serve as a biomarker for the disease onset.
