Introduction: DEMENTIA is basically the disease of old people which is usually caused by a primary degenerative lesion or by a structural disease in the brain. In terms of etiology, DEMENTIA is associated with reversible and irreversible causes. Determination of the underlying causes of DEMENTIA may facilitate its treatment and prognosis. The purpose of this study is to evaluate clinical and paraclinical symptoms of DEMENTIA as well as to determine the most common causes.Materials and Methods: This is a cross sectional descriptive study on 100 patients with DEMENTIA who referred to Shahrivar 17th Hospital in Mashhad. First, the patients who were diagnosed as being infected by DEMENTIA were evaluated according to DSM-IV criteria. They were also enrolled in history taking and physical examinations as well as paraclinical managements like EEG, CT Scan and MRI.The obtained data were then recorded down in the questionnaires.Results: 36% of the patients were females and 64% were males. Of this population, 43% had Alzheimer Disease (AD), 40% had VASCULAR DEMENTIA (VaD), 9% Parkinson disease (PD) and 8% had other types of DEMENTIA while there was no case of Ferontotemporal DEMENTIA (FTD). HTN, DM and Hyperlipidemia were found to have a fully significant effect on VaD.100% with the history of TIA and 88% with the history of CVA had VaD which was meaningful, too.55% of the VaD patients were identified with Gait disorder and 65% with Incontinence which is ststistically significant. Based on the results of MRI and CT Scan, 100% of the AD patients, 47.5% of the VaD patients and 88.9% of the PD patients were identified with cortical atrophy. In addition, it was found that hypocampus atrophy was present in 53.5% of the patients with AD and in 15% of the patients with VaD. In 90% of the VaD patients, hypodense foci was observed which is statistically significant, too.Conclusion: As the findings of the study suggest, the results of CT Scan and MRI was notably related to the type of DEMENTIA. Thus, it seems that using these two techniques can determine the existence of DEMENTIA in the early stages which can help with improving the quality and quantity of life in these patients. According to the frequency rate of VaD in our patients, it seems that the lack of or poor control of the risk factors like HTN, DM and hyperlipidemia can lead to the high frequency rate of VASCULAR DEMENTIA.

Background and Aim: VASCULAR DEMENTIA is one of the most common form of DEMENTIA. There is no treatment available to cure VASCULAR DEMENTIA or to alter clinical course. The aim of this study was to evaluate the effects of donepezil, memantine, rivastigmine and galantamine on mean flow velocity (MFV) and Mini-Mental State Examination (MMSE). Materials and Methods: This double-blind clinical trial was conducted on 44 patients with VASCULAR DEMENTIA. VASCULAR DEMENTIA was diagnosed based on the DSM-V criteria. According to the order of entry into the study, the participants were treated with one of the drugs (donepezil (10 mg/d), memantine 10 mg/d ), galantamine (8 mg/d) and rivastigmine6 mg/d. The sampling finished whenever 11 patients in each group completed the three-month trial. The MMSE and color Doppler ultrasound was performed for all participants before and three months after the intervention. Results: Our findings showed that memantine and donepezil significantly increased MMSE score (P = 0. 009 and P = 0. 001 respectively). Since there was no significant difference between the groups in the frequency of variables and the mean MMSE scores before the intervention, the administration of memantine and donepezil increased the MMSE scores. The findings also demonstrated that rivastigmine, galantamin and donepezil significantly increased MFV in some arteries. Conclusion: Memantine and donepazil improve cognitive function in patients with VASCULAR DEMENTIA. Rivastigmine, galantamin and donepezil increase MFV in some arteries although this effect seems limited.

Context: VASCULAR DEMENTIA (VaD) is the second most common type of DEMENTIA after Alzheimer’, s disease worldwide. VASCULAR DEMENTIA is a neurodegenerative disorder characterizedby gradual cognitive impairment. Ischemicandhemorrhagic strokes result in VaD, markedly distributing cerebral blood flow and decreasing patients’,cognitive and memory performance. Due to their high energy demands, neurons are more sensitive to cellular architecture changes and exposed to mitochondrial stress than other cell types. Mitochondrial dysfunction and selective autophagy of mitochondria, known as mitophagy, are associated with VaD. This review aims to elucidate the association between mitophagy and VaD. Evidence Acquisition: This review was conducted independently by at least two researchers dominant in various VaD studies. We searched databases including Elsevier, Google Scholar, and PubMed using the terms ‘, VASCULAR DEMENTIA’, , ‘, VASCULAR cognitive impairment’, , and ‘, mitophagy’, . We evaluated 70 articlesonthe relationship between VaDand mitophagy and interpreted the results. Adobe Photoshop 2022 was used for drawing figures by researchers. Results: The autophagy process plays a protective role in experimental VaD models via preserving VASCULAR integrity and the structure of the blood-brain barrier, upregulating occludin and claudin protein expressions, reducing oxidative stress, and decreasing cognitive dysfunction. Some studies claim that autophagy could have adverse effects in a time-dependent manner against neuronal injury. Prolonged autophagy and overexpressed autophagic proteins induce ischemic injury and cause neuronal cells to undergo apoptotic cell death. Conclusions: Although there are limited studies on the activation of mitophagy-related pathways in VaD, and the definitive role of mitophagy in neuronal healing is unclear, further research is needed to elucidate mitophagy pathways in neurons.

Chronic cerebral hypoperfusion (CCH) leads to VASCULAR DEMENTIA with progressive hippocampal damage and cognitive impairments. In the present study, we compared early and late Minocycline (MINO) treatment on cognitive function, long and short-term synaptic-plasticity following CCH. We used bilateral common carotid arteries occlusion model (2VO) for induction of hypoperfusion. Male Sprague-Dawley rats were divided into 5 following groups (each having 2 subgroups): 2VO + V (vehicle), 2VO+MINO-E (early treatment of MINO on days 0 to 3 after 2VO), 2VO+MINO-L (late-treatment on days 21 to 32 after 2VO), control, and sham. Passiveavoidance (PA) and radial arm maze (RAM) tests were used to investigate learning and memory. Long term and short term synaptic plasticity were assessed by field potential recording, the brains were removed after recording and preserved for histological study to count pyramidal cells in CA1 region. Cerebral hypoperfusion could impair memory performance, synaptic plasticity, and basal synaptic transmission (BST) along with hippocampal cell loss. Thus, we found a significant reduction in step-through latency (STL) of PA test with a higher number of working and reference errors in RAM in CCH rats. However, only late treatment with MINO improved memory performance, synaptic plasticity, hippocampal cell loss, and increased neurotransmitter pool (NP) in CCH rats, but early treatment could not produce long-lasting beneficial effects 32 days after 2VO. MINO may improve synaptic plasticity and memory performance in hypo-perfused rats directly and indirectly by increasing NP and/or suppressing inflammatory factors, respectively

Lysozyme amyloid aggregation is associated with VASCULAR DEMENTIA and other disorders. However, conventional therapies are limited by the blood-brain barrier. Gold nanoparticles (AuNPs) could modulate amyloid aggregation and provide a novel therapeutic approach. We investigated the effect of AuNPs on lysozyme amyloid formation of Hen Egg White Lysozyme (HEWL). We incubated lysozyme (3 mg/ml) in 60 mM glycine buffer (pH 2.8) at 61oC with gentle shaking to induce amyloid formation. We used various techniques to assess the impact of AuNPs (5-50 µg/ml) on lysozyme amyloid accumulation. We performed independent t-test and SPSS 23.0 software for data analysis. AuNPs inhibited lysozyme amyloid aggregation in a concentration-dependent manner. The lowest concentration (5 µg/ml) was the most effective, as it significantly increased the lag phase and decreased the growth phase of amyloid formation, and also reduced the cytotoxicity of amyloid aggregates on cell viability. Our results suggest that AuNPs act as nano-chaperones and prevent lysozyme amyloid fibril formation, and thus they may have therapeutic potential for VASCULAR DEMENTIA treatment.