Vascular Dementia

Uncaria species (Gouteng in Chinese) have been used as a plant medicine to treat ailments of cardiovascular and central nervous systems. As the main alkaloid constituent of Uncaria species, isorhynchophylline has drawn extensive attention toward antihypertensive and neuroprotective activities in recent years. Isorhynchophylline mainly acts on cardiovascular and central nervous systems diseases including hypertension, brachycardia, arrhythmia, and sedation, vascular dementia, and amnesia. Isorhynchophylline also has effects on anticoagulation, inhibition vascular smooth muscle cell apoptosis and proliferation, anti-multidrug resistant of lung cells, anti-endotoxemic, and antispasmodic. The active mechanisms are related to modulation on calcium ion channel, protection neural and neuroglial cells against -amyloid(25-35)-induced neurotoxicity and via inducing autophagy. As a candidate drug of several cardiovascular and central nervous systems diseases, isorhynchophylline will attract

Assess the contribution of structural and functional neuroimaging methods to the diagnosis of dementia.|This was a retrospective chart and imaging review. Participants were 24 inpatient dementia cases from a general hospital-based, university medical psychiatry unit. Data from clinical charts and imaging results were reviewed.|Most common initial diagnoses were dementia NOS and vascular dementia (VD); most common discharge diagnoses were VD, Alzheimer's, Dementia NOS and dementia with Lewy bodies. Most diagnostic changes occurred following family meetings or SPECT/PET, with fewer changes after CT/MRI.|Diagnostic steps that contributed the most to the final diagnosis were the family meeting and the functional neuroimaging evaluation.

Cerebrovascular disease is recognized as a common cause of cognitive impairment and dementia, alone or coexisting with other neurodegenerative diseases, mostly Alzheimer's disease. Vascular cognitive impairment (VCI) is a part of the heterogenous disorders group related to cerebral vessel disease. Although age is one of the most important risk factors for VCI, other common cardiovascular risk factors are also involved. By investigating these risk factors, a high proportion of these cognitive disorders can be prevented and/or delayed. Until now, only treatment of midlife arterial hypertension has been recognized as a preventing factor of vascular dementia. Brain MRI is becoming the method of choice to investigate cerebral vascular pathologies. However, this form of morphological imaging remains inadequate and does not provide useful functional information during VCI exploration, despite which functional imaging such as brain perfusion single-photon computed tomography, performed in

Alzheimer's disease (AD) and cerebrovascular disorders are the leading causes of dementia in our ageing population. Given that the progression of neuropathological changes in the brains of AD patients initiates several years, and even decades, before the diagnosis of dementia, a great effort has been made to identify potentially modifiable factors that contribute to the pathogenesis of sporadic late-onset AD. Among these factors, cerebrovascular disease and microvascular alterations seem to bilaterally interact with the underlying AD pathology, affecting the progression of cognitive deficits. In addition, cerebrovascular dysfunction has emerged as an early event in AD, encompassing changes in virtually all cell types of the neurovascular unit, including bone marrow-derived cells, astrocytes, pericytes, vascular smooth muscle cells and endothelial cells. In this review, we discuss recent studies implicating cerebrovascular factors in the pathogenesis of AD. We also discuss how the

Schizophrenia (SZP) has been historically referred to as "dementia praecox" because of the recognition that its onset is associated with deficits in memory, attention and visuospatial orientation. We wondered whether there is evidence for additional cognitive decline late in the course of chronic SZP. This review examined the evidence (1) for cognitive decline late in the course of chronic SZP, (2) for how often the late cognitive decline occurs, and (3) whether the cognitive decline in late-life SZP is related to pathophysiology of SZP versus the superimposition of another type of dementia. A PUBMED search was performed combining the MESH terms schizophrenia and dementia, cognitive decline, cognitive impairment and cognitive deficits. A manual search of article bibliographies was also performed. We included longitudinal clinical studies employing standard tests of cognition. Cross-sectional studies and those that did not test cognition through standard cognitive tests were excluded.

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Dementia.