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Cerebrovascular disease (CVD) is an important cause of psychiatric disability in the elderly. Much of this disability can be attributed to dementia and lesser degrees of cognitive impairment, which result from strokes and other forms of cerebrovascular pathology. While vascular dementia is common, estimates of its frequency vary due to its clinical and pathologic heterogeneity, the challenges involved in its measurement and its frequent co-occurrence with Alzheimer's disease. Nevertheless the clinical features and natural histories of vascular dementia can be described, and risk factors have been identified and include hypertension, diabetes mellitus, hyperlipidaemia, other conditions that promote atherosclerosis, and rare genetic mutations. While vascular dementia is not curable, treatments are available. For example, a few recent clinical trials suggest that cholinesterase inhibitors have some efficacy. Our knowledge of the risk factors has also provided opportunities for the primary and secondary prevention of vascular dementia, and indicates promising avenues for research.
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PMID:Cerebrovascular disease and dementia. 1708 61

Prior work has suggested that obesity and overweight as measured by body mass index (BMI) increases risk of dementia. It is unknown if there is a difference in the risk of developing Alzheimer disease (AD) versus vascular dementia (VaD) associated with high body weight. The goal of this study was to examine the association between midlife BMI and risk of both AD and VaD an average of 36 years later in a large (N= 10,136) and diverse cohort of members of a health care delivery system. Participants aged 40-45 participated in health exams between 1964 and 1968. AD and VaD diagnoses were obtained from Neurology visits between January 1, 1994 and June 15, 2006. Those with diagnoses of general dementia from primary care providers were excluded from the study. BMI was analyzed in WHO categories of underweight, overweight and obese, as well as in subdivisions of WHO categories. All models were fully adjusted for age, education, race, sex, marital status, smoking, hyperlipidemia, hypertension, diabetes, ischemic heart disease and stroke. Cox proportional hazard models showed that compared to those with a normal BMI (18.5-24.9), those obese (BMI > or = 30) at midlife had a 3.10 fold increase in risk of AD (fully adjusted model, Hazard Ratio=3.10, 95% CI 2.19-4.38), and a five fold increase in risk of VaD (fully adjusted model, HR=5.01, 95% CI 2.98-8.43) while those overweight ( BMI > or = 25 and <30) had a two fold increase in risk of AD and VaD (fully adjusted model, HR=2.09, 95% CI 1.69-2.60 for AD and HR=1.95, 95% CI 1.29-2.96 for VaD). These data suggest that midlife BMI is strongly predictive of both AD and VaD, independent of stroke, cardiovascular and diabetes co morbidities. Future studies need to unveil the mechanisms between adiposity and excess risk of AD and VaD.
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PMID:Body mass index in midlife and risk of Alzheimer disease and vascular dementia. 1743 Feb 31

Alzheimer's disease (AD) is considered to be the most common dementing disorder. The understanding of this disorder has greatly advanced over the past few years, and new therapeutic options have been developed. Another disorder, vascular dementia (VaD), is a syndrome with multiple etiologies operating through a variety of different mechanisms. The combination of AD and VaD is extremely common, making mixed dementia the most common type of dementia. Risk factors for VaD, which are the common vascular risk factors, are presently known to apply also to AD. Cholinergic deficits occur in both conditions. The identification of several genetic factors that can contribute to vascular damage, as well as possible auto-immune damage to vascular components, are important. It is remarkable that amyloid precursor protein (APP) mutations can cause the typical pathological changes of AD as well as amyloid deposition around blood vessels. These may lead to deficient blood perfusion to the brain, changes of the blood-brain barrier, as well as cerebral hemorrhages. Interestingly, attention to risk factors, such as hypertension, coronary artery disease, hyperlipidemia and smoking could reduce or delay the incidence of dementia, both vascular and AD.
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PMID:The prevention of the dementia epidemic. 1749 Jun 85

Essential hypertension can be defined as a rise in blood pressure of unknown cause that increases risk for cerebral, cardiac, and renal events. In industrialised countries, the risk of becoming hypertensive (blood pressure >140/90 mm Hg) during a lifetime exceeds 90%. Essential hypertension usually clusters with other cardiovascular risk factors such as ageing, being overweight, insulin resistance, diabetes, and hyperlipidaemia. Subtle target-organ damage such as left-ventricular hypertrophy, microalbuminuria, and cognitive dysfunction takes place early in the course of hypertensive cardiovascular disease, although catastrophic events such as stroke, heart attack, renal failure, and dementia usually happen after long periods of uncontrolled hypertension only. All antihypertensive drugs lower blood pressure (by definition) and this decline is the best determinant of cardiovascular risk reduction. However, differences between drugs exist with respect to reduction of target-organ disease and prevention of major cardiovascular events. Most hypertensive patients need two or more drugs for blood-pressure control and concomitant statin treatment for risk factor reduction. Despite the availability of effective and safe antihypertensive drugs, hypertension and its concomitant risk factors remain uncontrolled in most patients.
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PMID:Essential hypertension. 1770 55

Alzheimer's disease (AD) is the most common cause of dementia affecting nearly 18 million people around the world and 4.5 million in the US. It is a progressive neurodegenerative condition that is estimated to dramatically increase in prevalence as the elderly population continues to grow. As the cognitive and neuropsychiatric signs and symptoms of AD progresses in severity over time, affected individuals become increasingly dependent on others for assistance in performing all activities of daily living. The burden of caring for someone affected by the disorder is great and has substantial impact on a family's emotional, social and financial well-being. In the US, the currently approved medications for the treatment of mild to moderate stages of AD are the cholinesterase inhibitors (ChEIs). Cholinesterase inhibitors have shown modest efficacy in terms of symptomatic improvement and stabilization for periods generally ranging from 6 to 12 months. There are additional data that have emerged, which suggest longer-term benefits. For the moderate to severe stages of AD, memantine, an N-methyl-D-aspartate (NMDA) receptor antagonist is in widespread use and has shown modest benefit as monotherapy and in combination with ChEIs. The cost effectiveness of the currently available therapeutic agents for AD has undergone great scrutiny and remains controversial, especially outside the US. Neuropsychiatric symptoms such as agitation and psychosis are common in AD. Unfortunately, in the US there are no Food and Drug Administration (FDA)-approved agents for the treatment of these symptoms, although atypical antipsychotics have shown some efficacy and have been widely used. However, the use of these agents has recently warranted special caution due to reports of associated adverse effects such as weight gain, hyperlipidemia, glucose intolerance, cerebrovascular events, and an increased risk for death. Alternative agents used to treat neuropsychiatric symptoms include serotonergic antidepressants, benzodiazepines, and anticonvulsant medications.
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PMID:Treatment of Alzheimer's disease across the spectrum of severity. 1804 10

Attention to the role of n-3 long-chain fatty acids in human health and disease has been continuously increased during recent decades. Many clinical and epidemiologic studies have shown positive roles for n-3 fatty acids in infant development; cancer; cardiovascular diseases; and more recently, in various mental illnesses, including depression, attention-deficit hyperactivity disorder, and dementia. These fatty acids are known to have pleiotropic effects, including effects against inflammation, platelet aggregation, hypertension, and hyperlipidemia. These beneficial effects may be mediated through several distinct mechanisms, including alterations in cell membrane composition and function, gene expression, or eicosanoid production. A number of authorities have recently recommended increases in intakes of n-3 fatty acids by the general population. To comply with this recommendation a variety of food products, most notably eggs, yogurt, milk, and spreads have been enriched with these fatty acids. Ongoing research will further determine the tissue distribution, biological effects, cost-effectiveness, and consumer acceptability of such enriched products. Furthermore, additional controlled clinical trials are needed to document whether long-term consumption or supplementation with eicosapentaenoic acid/docosahexaenoic acid or the plant-derived counterpart (alpha-linolenic acid) results in better quality of life.
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PMID:A systemic review of the roles of n-3 fatty acids in health and disease. 1932 62

The incidence of dementia is increasing dramatically with the ageing population. Increasing evidence indicates that vascular disease is associated with cognitive decline and with the most common form of dementia, Alzheimer's disease (AD). Cardiovascular risk factors such as hyperlipidaemia, hypertension and type 2 diabetes have attracted attention as potential targets in the prevention of dementia. The present review aims to provide a concise overview of the recent advances linking vascular disease with dementia (with a particular focus on AD) and to examine the evidence for efficacy, where possible, for utilising vascular pharmacotherapy as a treatment option for dementia.
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PMID:Vascular pharmacotherapy and dementia. 1948 34

It has become increasingly apparent, especially with the advent of MRI brain scanning, that a large number of patients develop signal intensity changes in the subcortical white matter and periventricular region as they age. This appears to be accelerated by risk factors for small vessel cerebrovascular disease such as hypertension, smoking, diabetes mellitus and hyperlipidemia. The major question becomes when such changes become clinically significant. It is obvious that subcortical lacunar-type infarction can be identified by the clinical presentation. For example, typical examples of so-called "lacunar syndrome" include pure motor hemiparesis, pure sensory stroke, sensorimotor stroke, clumsy hand-dysarthria, and hemiataxia-hemiparesis. The issue becomes a measure of impact on functional ability. This is influenced by several factors. Baseline IQ and educational level, as well as expectations of age, certainly play a role. A person who develops cognitive impairment and long tract signs in their 50s or 60s is certainly going to be recognized as more impaired than an 80 year old individual who is retired and primarily is engaged in recreational activity. It would be expected that a person born with limited intellectual capacity and/or limited educational opportunity would be less likely to be identified as impaired than a person who has achieved substantial economic achievement through their innate talents. The concept of tissue loss or lesion load becomes important when determining how pronounced the ischemic cerebrovascular changes translate into functional impairment. Correlative pathology may include cortical atrophy and ventricular dilatation. Loss of either cortical or subcortical tissue function is expected to be related to functional compromise. In addition, there are potential features such as the coexistence of small vessel cerebrovascular disease and Alzheimer's disease. Small vessel cerebrovascular disease might also play a contributing factor in patients susceptible to Dementia with Lewy Bodies or patients susceptible to fronto-temporal dementia or any other dementing process. Thus, the concept of tissue loss or lesion burden of disease becomes increasingly important as we recognize the potential for multifactorial issues, including genetic factors, to contribute to the phenotypic expression. The relationships between cognitive impairment, dementia and subcortical vascular lesions are poorly understood. There have been several papers on the different aspects of cerebral insults and their impact on cognition, the various kinds of dementia and different methods of analyzing the impact of the various insults to the brain. This chapter is an attempt to review all pertinent information currently available on the poorly understood condition of "subcortical ischemic cerebrovascular dementia."
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PMID:Subcortical ischemic cerebrovascular dementia. 1950 11

Dementia is an important public health problem of increasing magnitude. At present, available therapies provide only minor and temporary relief, and attempts to find a cure have so far failed. Epidemiological studies have identified risk factors for dementia, particularly Alzheimer's disease and vascular dementia. In principle, these findings provide an opportunity to intervene and prevent the dementia epidemic. Attention to nongenetic risk factors such as hypertension, hyperlipidemia, smoking, and obesity may thus not only prevent cardiovascular disease but also dementia, although it is difficult to prove the efficacy of these measures for dementia prevention.
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PMID:Is dementia preventable? 1958 56

Vascular cognitive impairment (VCI) is the phenotypic outcome of a cascade of events: vascular risk factors lead to vascular disease, which causes vascular brain injury (VBI) in networks important for cognition. Both VCI and Alzheimer's disease (AD) increase exponentially with age, and their interactions are common and controversial. The ability of current consensus criteria to distinguish VCI from AD is limited. Currently, the primary and secondary prevention of VCI is essentially the same for stroke, whereas symptomatic treatment of VCI is similar to AD. An emerging database suggests that VBI contributes significantly to mild VCI and can accelerate the appearance of dementia when AD pathology is mild. Early evidence suggests that the adverse effects of VBI are submerged once AD pathology spreads into isocortex. Recently, epidemiologic studies reported associations between vascular risk factors and clinically diagnosed AD as well as stroke. If hypertension, diabetes, and hyperlipidemia truly accelerate beta-amyloidosis and tauopathy, as well as VBI, the importance of their early identification and treatment will be greatly magnified.
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PMID:Vascular cognitive impairment: today and tomorrow. 1959 88


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