Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prevalence of dementing illnesses is expected to grow due to aging of the population throughout the world. Vascular dementia and Alzheimer's disease share several risk factors and are nowadays considered two ends of a continuum rather than two distinct entities. Traditional cardiovascular risk markers such as diabetes, dyslipidemia, hypertension, metabolic syndrome and adiposity in mid-life are harbingers of cognitive decline, Alzheimer's disease and vascular dementia later in life. In aged populations, only diabetes has been more constantly associated with the development of cognitive dysfunction, while other risk markers have shown more mixed results. Normal aging, co-morbidities and other changes connected to cognitive decline make the interpretation of the risk markers in the elderly challenging and probably explain these contradictory findings. Control of cardiovascular risk factors has been linked to beneficial effects in terms of cognition in cross-sectional and prospective follow up studies, but the results of interventional trials have been disappointing. More research in this area is needed, specifically, placebo-controlled randomized trials in both mid-life and late-life with cognitive dysfunction as a primary endpoint.
...
PMID:The complex interplay of cardiovascular system and cognition: how to predict dementia in the elderly? 2109 51

Vascular dementia (VAD), the second most common form of dementia after Alzheimer's disease (AD) is characterized by a cognitive deficit of cerebrovascular origin. As for AD, the main proposed treatment is based on cholinesterase inhibitors. However, randomized clinical trials (RCTs) with cholinesterase inhibitors in VAD reported modest - though sometimes statistically significant - clinical efficacy. Non-cholinergic drugs with diverse rationales and mechanisms of action have also been tested in a few RCTs for VAD; the outcomes measured are variable and the evidence of efficacy is weak. The limitations of pharmacological treatment for VAD have prompted a different strategy, i.e. primary prevention aimed at reducing vascular risk factors. Several epidemiological studies reported associations of hypertension, type 2 diabetes, obesity, and inflammation with VAD and in some cases, AD. These all coincide with those of stroke, which in turn is an established factor for cognitive decline and VAD. Here too, only a few RCTs have looked at prevention of these factors, except hypertension. Some pharmacological classes are particularly promising from the clinical and experimental viewpoints: Ca2+ channel blockers and drugs affecting the renin-angiotensin system may act independently of the effects on blood pressure. Despite some conflicting results and the need for further work, the control of risk factors might prevent cognitive decline and VAD in the elderly. The benefit of tackling vascular factors is probably larger when also considering the prevention of stroke. The objective of this review is to analyze the pharmacological treatment and prevention of VAD and their outcome. The literature on Pubmed from 1980 to 2009 was examined.
...
PMID:Pharmacotherapy and prevention of vascular dementia. 2129 2

Cognitive impairment due to cerebrovascular disease is termed "Vascular Cognitive Impairment" (VCI) and forms a spectrum that includes Vascular Dementia (VaD) and milder forms of cognitive impairment referred to as Vascular Mild Cognitive Impairment (VaMCI). VCI represents a complex neurological disorder that occurs as a result of interaction between vascular risk factors such as hypertension, diabetes, obesity, dyslipidemia, and brain parenchymal changes such as macro and micro infarcts, haemorrhages, white matter changes, and brain atrophy occurring in an ageing brain. Mixed degenerative and vascular pathologies are increasingly being recognised and an interaction between the AD pathology, vascular risk factors, and strokes is now proposed. The high cardiovascular disease burden in India, increasing stroke incidence, and ageing population have contributed to large numbers of patients with VCI in India. Inadequate resources coupled with low awareness make it a problem that needs urgent attention, it is important identify patients at early stages of cognitive impairment, to treat appropriately and prevent progression to frank dementia.
...
PMID:Vascular cognitive impairment: Current concepts and Indian perspective. 2136 14

Vascular dementia (VaD) is common. Pure vascular disease may account for 5-20% of all cases of dementia, while mixed dementia, Alzheimer's disease (AD) with VaD, occurs at least as frequently. There is no specific treatment or cure for VaD, but its proximity to other conditions may make it amenable to interventions at various stages. The causes of VaD are multifactorial and involve neuronal networks needed for memory and cognition, executive function and behaviour. Hypertensive angiopathy is the major known causative factor for VaD. Recent research suggests that VaD and AD occupy ends of the same spectrum and share common risk factors. As VaD is closely related to cardiovascular disease, modifying cardiovascular risk factors may assist in its prevention. Hypertension in midlife increases the risk of all-cause dementia. Regular screening of high-risk individuals could help to detect dementia early on enabling appropriate preventive intervention. Medication for hypertension, diabetes, and hypercholesterolaemia is recommended. Behavioural treatments include enhancing and encouraging cognitive and physical activity, social engagement, smoking cessation and healthy diet, including alcohol reduction. Comorbid depression is common in older people with dementia and treating this can improve cognition. Typically, patients are in their late sixties or early seventies, and may present after a cerebrovascular event. The onset is usually more acute than that of AD. Typical signs and symptoms are gait disturbance, unsteadiness and falls, urinary symptoms not explained by urological disease, pseudobulbar palsy and personality and mood changes. Insight is preserved until late in the disease and seizures or other manifestations of cerebral ischaemic accidents are not infrequent. VaD is characterised by stepwise deterioration with periods of partial recovery that can last months between periods of deterioration and cognitive decline.
...
PMID:Diagnosing and managing vascular dementia. 2272 Apr 54

Vascular dementia (VaD) is a common dementing illness. There are no pharmacological agents with a regulatory approval for its treatment or prevention. Review of published clinical trial reports indicates that early treatment of hypertension, a risk factor for stroke, reduces VaD risk and slows progression. However, unlike stroke, treatment of hyperlipidemia with statin class drugs or treatment of blood clotting abnormalities with acetylsalicylic acid do not appear to have an effect on VaD incidence or progression. Pharmacological agents for treatment of Alzheimer's dementia (AD) such as memantine or acetylcholinesterase inhibitors have small positive effects on cognition in VaD, which are likely due to their action on co-existing AD-related neuropathology. Drug development efforts using novel approaches such as patient stratification by their genotype are needed in order to address the increasing need for effective VaD therapeutics.
...
PMID:Pharmacological prevention and treatment of vascular dementia: approaches and perspectives. 2279 25

In recent years, accumulating evidence has suggested that vascular risk factors (especially hypertension, and also diabetes, high level of cholesterol and smoking) contribute to Alzheimer disease. Vascular dementia had been traditionally considered secondary to stroke and vascular disease. However it appears that there is a continuous spectrum of disease, composed of a gradient of features of both types of dementia. The brain is an early target for organ damage due to high blood pressure. Hypertension is the major modifiable risk factor for stroke and small vessel disease and is known to be the most-important factor for macrovascular cerebral complications such as atherotrombotic stroke and, consequently, vascular dementia. Hypertension may also predispose to more subtle cerebral processes based on arteriolar narrowing or microvascular pathological changes. The term cerebral small vessel disease refers to a group of pathological processes with various etiologies that affect the small arteries, arterioles, venules, and capillaries of the brain. Age-related and hypertension-related small vessel diseases and cerebral amyloid angiopathy are the most common forms. It has been suggested that cerebral microvascular disease contributes to vascular cognitive impairment. The mechanisms underlying hypertension-related cognitive changes are complex and not yet fully understood. Both high and, especially in the elderly, low blood pressure have been linked to cognitive decline and dementia. There is some evidence that antihypertensive drug treatment could play a role in the prevention of cognitive impairment or vascular dementia through BP control. The BP levels that should be targeted to achieve optimal perfusion while preventing cognitive decline are still under debate.
...
PMID:Cerebral small vessel disease, cognitive impairment and vascular dementia. 2280 35

Cognitive disorders are likely to increase over the coming years (5-10). Vascular dementia (VaD) has heterogeneous pathology and is a challenge for clinicians. Current Alzheimer's disease drugs have had limited clinical efficacy in treating VaD and none have been approved by major regulatory authorities specifically for this disease. Role of iNOS and NADPH-oxidase has been reported in various pathological conditions but there role in hypertension (Hypt) induced VaD is still unclear. This research work investigates the salutiferous effect of aminoguanidine (AG), an iNOS inhibitor and 4'-hydroxy-3'-methoxyacetophenone (HMAP), a NADPH oxidase inhibitor in Hypt induced VaD in rats. Deoxycorticosterone acetate-salt (DOCA-S) hypertension has been used for development of VaD in rats. Morris water-maze was used for testing learning and memory. Vascular system assessment was done by testing endothelial function. Mean arterial blood pressure (MABP), oxidative stress [aortic superoxide anion, serum and brain thiobarbituric acid reactive species (TBARS) and brain glutathione (GSH)], nitric oxide levels (serum nitrite/nitrate) and cholinergic activity (brain acetyl cholinesterase activity-AChE) were also measured. DOCA-S treated rats have shown increased MABP with impairment of endothelial function, learning and memory, reduction in serum nitrite/nitrate & brain GSH levels along with increase in serum & brain TBARS, and brain AChE activity. AG as well as HMAP significantly convalesce Hypt induced impairment of learning, memory, endothelial function, and alterations in various biochemical parameters. It may be concluded that AG, an iNOS inhibitor and HMAP, a NADPH-oxidase inhibitor may be considered as potential agents for the management of Hypt induced VaD.
...
PMID:Pharmacological inhibition of inducible nitric oxide synthase (iNOS) and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, convalesce behavior and biochemistry of hypertension induced vascular dementia in rats. 2320 48

The increasing prevalence of dementia with age, combined with the rapid aging of the population, heralds an oncoming epidemic of dementia in industrialized countries. The current prevalence of dementia over 65 years of age is close to 7% (2/3 Alzheimer's disease and 1/3 vascular dementia). Vascular dementia refers to a severe cognitive decline due to brain lesions of vascular origin. It is in fact a heterogeneous syndrome with multiple etiopathogenic varieties such as subcortical small artery disease, isolated strategic stroke, multiple infarcts, chronic cerebral hypoperfusion, and amyloid angiopathy. Vascular dementia classically occurs or worsens abruptly and has a subcortical pattern of cognitive impairment, contrasting with the gradual cortical dementia of Alzheimer's disease. Recent data, including the results of neuro-imaging studies, show however that this classical opposition is no longer justified and that most dementias are "mixed", with a synergy between Alzheimer's disease lesions and vascular risk factors going from, silent brain lesions of vascular origin, to at most, clinically patent strokes. The main therapeutic implication is that, in the absence of effective methods for Alzheimer's disease prevention, the best way to prevent dementia in general is to prevent strokes, based primarily on early treatment of vascular risk factors, particularly hypertension.
...
PMID:[Vascular dementia]. 2342 Sep 60

Vascular dementia is caused by various factors, including increased age, diabetes, hypertension, atherosclerosis, and stroke. Adiponectin is an adipokine secreted by adipose tissue. Adiponectin is widely known as a regulating factor related to cardiovascular disease and diabetes. Adiponectin plasma levels decrease with age. Decreased adiponectin increases the risk of cardiovascular disease and diabetes. Adiponectin improves hypertension and atherosclerosis by acting as a vasodilator and antiatherogenic factor. Moreover, adiponectin is involved in cognitive dysfunction via modulation of insulin signal transduction in the brain. Case-control studies demonstrate the association between low adiponectin and increased risk of stroke, hypertension, and diabetes. This review summarizes the recent findings on the association between risk factors for vascular dementia and adiponectin. To emphasize this relationship, we will discuss the importance of research regarding the role of adiponectin in vascular dementia.
...
PMID:Association between risk factors for vascular dementia and adiponectin. 2486 Aug 14

Vascular dementia is a devastating disorder not only for the patient, but also for the family because this neurocognitive disorder breaks the patient's independence, and leads to family care of the patient with a high cost for the family. This complex disorder alters memory, learning, judgment, emotional control and social behavior and affects 4% of the elderly world population. The high blood pressure or arterial hypertension is a major risk factor for cerebrovascular disease, which in most cases leads to vascular dementia. Interestingly, this neurocognitive disorder starts after long lasting hypertension, which is associated with reduced cerebral blood flow or hypoperfusion, and complete or incomplete ischemia with cortical thickness. Animal models have been generated to elucidate the pathophysiology of this disorder. It is known that dendritic complexity determines the receptive synaptic contacts, and the loss of dendritic spine and arbor stability are strongly associated with dementia in humans. This review evaluates relevant data of human and animal models that have investigated the link between long-lasting arterial hypertension and neural morphological changes in the context of vascular dementia. We examined the effect of chronic arterial hypertension and aged in vascular dementia. Neural dendritic morphology in the prefrontal cortex and the dorsal hippocampus and nucleus accumbens after chronic hypertension was diskussed in the animal models of hypertension. Chronic hypertension reduced the dendritic length and spine density in aged rats.
...
PMID:Neuronal changes after chronic high blood pressure in animal models and its implication for vascular dementia. 2678 33


<< Previous 1 2 3 4 5 Next >>