Tau protein in neurodegenerative diseases - a review.

The study of rare, inherited forms of different diseases resulted in the discovery of gene defects that cause inherited variants of the respective diseases. The defective genes were found to encode major molecular players leading to the neuropathological lesions or factors that characterize these diseases. The exact role of the tau protein in the neurodegenerative process is still under debate. It is very important to understand the normal biological roles of tau and the specific events that induce tau to become neurotoxic. Tau is the major microtubule-associated protein (MAP) of a mature neuron. The other neuronal MAPs are MAP1 and MAP2. These three MAPs perform similar function, promoting assembly and stability of microtubules. Tau protein was isolated as a microtubule-associated factor in the porcine brain. It was isolated as a protein that co-purified with tubulin and had the ability to promote microtubule assembly in vitro. Normal adult human brain tau contains 2-3 moles phosphate÷mole of tau protein. Hyperphosphorylation of tau depress this biological activity of tau. Almost 80 diseases caused by missense mutations and intronic mutations in the tau gene have been found in familial cases of frontotemporal dementia (FTD). In Alzheimer's disease (AD), there are intraneuronal neurofibrillary tangles composed of the microtubule-associated protein tau (MAPT). In other neurodegenerative diseases, there are similar deposits of tau, in the absence of extracellular deposits (progressive supranuclear palsy, corticobasal degeneration, argyrophilic grain disease, etc.). Tau pathology is also often seen in some forms of Parkinson's disease (PD) and prion diseases. In genetic forms of FTD, mutations in tau implicate abnormal tau as the initiation of neurodegeneration. In FTD, there are deposits especially in temporal and frontal lobes, regions that are very important for behavior and executive function. It is critical to understand how tau becomes pathogenic, in order to consider developing any strategies for treatment.

Study on cognitive decline in patients diagnosed with brain tumors.

AIM: The purpose of our study was to assess the cognitive performance in patients with primitive brain tumors and to analyze the cognitive status of these patients, correlated with histological type of brain tumors. PATIENTS, MATERIALS AND METHODS: The study enrolled 52 patients diagnosed with primitive brain tumors, hospitalized in Neuropsychiatry Hospital of Craiova, Romania, from December 2013 to December 2015. According to the histological type of tumors, the patients were classified into three groups: Group A included 22 patients with meningioma, Group B composed of 16 patients diagnosed with glioblastoma, and Group C including 14 patients diagnosed with diffuse astrocytoma. Neurological examination, neuroimaging assessment [computed tomography (CT) or magnetic resonance imaging (MRI) for skulls] to diagnose primitive brain tumors, then the confirmation of clinical and histopathological diagnoses were performed for these patients. For cognitive assessment performed before surgery, Montreal Cognitive Assessment (MoCA) and Cambridge Cognitive Examination (CAMCOG) scales were used. The results were statistically analyzed using the Student's t-test; p-values less than 0.05 were considered statistically significant. RESULTS: In terms of age, we did not observe statistically significant differences between the three groups of patients. The group of patients with diffuse astrocytoma presented a higher educational level compared to patients with glioblastoma or meningioma. MoCA score obtained in glioblastoma group was 21.7 points, while in the group of patients with diffuse astrocytoma was 23.5 points, and in the group of patients with meningioma 24.2 points. The cognitive assessment using CAMCOG scale led to the following results: group of patients diagnosed with glioblastoma showed an average score of 83.5 points, the diffuse astrocytoma group had an average score of 88.9 points and the group with meningioma an average score of 90.1 points. CONCLUSIONS: Patients diagnosed with glioblastoma showed a statistically significant cognitive decline in comparison to patients diagnosed with diffuse astrocytoma (p<0.05). We did not notice statistically significant differences in the cognitive decline of patients with meningioma compared to those diagnosed with diffuse astrocytoma (p>0.05).