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The Scale of the Problem—Overweight and Obesity
Published in Ruth Chambers, Paula Stather, Tackling Obesity and Overweight Matters in Health and Social Care, 2022
In the general UK population, around a quarter of the population are classed as ‘inactive’—that is, not even achieving a minimum of 30 minutes of activity per week.7 Physical inactivity is the fourth largest cause of disease and disability in the UK. Staying active can reduce the risk of vascular dementia, too, and has a positive impact on non-vascular dementia. It’s common for around two fifths of adults in the UK to spend more than six hours a day desk-bound or sitting still.
Introduction to dementia
Published in Joanne Brooke, Dementia in Prison, 2020
Vascular dementia is caused by the death of cells in the brain from a reduced blood supply due to damaged blood vessels (National Health Service, 2020). A healthy brain functions when brain cells have a constant supply of blood, which conveys oxygen and nutrients. When the blood supply is interrupted, the death of brain cells occurs. This can be caused by three main aetiological reasons. First, when narrowing of the small blood vessels occurs deep within the brain, this type of dementia is subcortical vascular dementia or small vessel disease. Second, when blood supply to a part of the brain suddenly stops due to a clot in a blood vessel, this is a stroke, and dementia that occurs after a stroke is referred to as post-stroke dementia or single-infarct dementia. Third, similar to a stroke, but incomplete strokes, transient ischaemic attacks (TIAs) can cause damage across the brain, which is referred to as multi-infarct dementia (NHS, 2020).
Estrogens and dementia: a clinical and epidemiological update
Published in Barry G. Wren, Progress in the Management of the Menopause, 2020
Ischemic stroke elevates the risk of dementia17, where dementia is usually attributed to the accumulation of multiple infarcts in subcortical and cortical regions of the cerebral hemispheres and in the brain stem. Appropriately, the typical form of vascular dementia is referred to as multi-infarct dementia. Whereas Alzheimer’s disease symptoms are almost imperceptible at their onset, vascular dementia is more often characterized by the abrupt onset of cognitive impairments. Symptoms progress in a stepwise fashion, contrasting with the more gradual worsening of Alzheimer’s disease. Although the cognitive profiles can differ in these two dementing disorders, vascular dementia is usually distinguished on the basis of its saltatory clinical course, associated signs of focal neurological disturbance (e.g. hemiparesis), and brain imaging studies that confirm the presence of infarction. The most important riskfactor for vascular dementia is hypertension”. Interestingly, the c4 allele of apolipoprotein E may be linked to a greater risk of cerebrovascular disease19, in addition to its more firmly established association with Alzheimer’s disease.
Impact of cerebral microbleeds on cognitive functions and its risk factors in acute cerebral infarction patients
Published in Neurological Research, 2023
Linyun Chen, Feng Liu, Xuan Tian, Tian Zhang, Jian Zhang, Fang Ran
At present, the number of patients with vascular dementia is increasing year by year. It is the second most common cause of dementia after Alzheimer’s disease [32]. Vascular dementia is the only dementia that can control the progression of the disease and even achieve clinical recovery through early diagnosis and early treatment [33]. Different from acute and chronic cerebral hemorrhage, CMBs are a product of vascular degeneration or a pathological state with hemorrhagic tendency [15]. Whether CMBs cause cognitive impairment independently of white matter damage and critical cerebral infarction is unclear. However, a large number of studies have shown that cerebral microbleeds are significantly correlated with cognitive dysfunction in areas such as attention and memory, visuospatial executive ability, and so on [10]. At present, the mechanism of CMB-induced cognitive dysfunction remains controversial [29]. The main mechanism theory mainly includes the destruction of frontal-subcortical cholinergic circuit and the deposition of hemosiderin and β-amyloid. In addition, it has been reported that cognitive impairment caused by CMBs is related to the location and number of CMBs. Some studies suggest that cognitive impairment is related to lobar microbleeds, and some studies suggest that it is related to deep white matter microbleeds [22]. Regardless of the mechanism by which CMBs lead to cognitive impairment, our study has demonstrated that serum D-dimer, serum hs-CRP, serum NSE, and serum S100β are all related to the occurrence of CMBs.
Calcified carotid artery atheromas in individuals with cognitive dysfunction
Published in Acta Odontologica Scandinavica, 2023
Anton Jonsson, Jacob Holmer, Leif Kullman, Maria Eriksdotter, Jan Ahlqvist, Eva Levring Jäghagen, Kåre Buhlin
Previous research indicates a higher prevalence of CVD in patients with dementia than in cognitively healthy controls [9,22,23]. The present study did not find significant differences in the prevalence of CCAA among patients suffering from AD, the cognitive impairment subgroups and controls. There are several possible explanations for this observation. First, those diagnosed with AD, MCI and SCD had visited a memory clinic and undergone a thorough medical evaluation in which CVD may have been diagnosed and treated. Second, the cardiovascular health of the members in the control group was based on anamnestic data and they could potentially have undiagnosed CVD that manifested as CCAA. This self-reported health declaration by the controls is a limitation of this study. Furthermore, the studies referred to above included subjects with vascular dementia. In our study, patients suffering from vascular dementia were excluded because the aim was to investigate a possible association between non-vascular dementia and CCAA. It is likely that exclusion of these patients led to fewer participants with CCAA in our study population. In this context, the burden of CCAA is no greater in individuals with AD than in cognitively healthy subjects.
Event- and time-based prospective memory in hemodialysis patients
Published in Renal Failure, 2020
Bin Wang, Mengting Li, Fang Tang, Yue Wang, Yuchen Han, Wen Lu, Lan Zhang, Ling Zhang, Weijie Ni, Li Zhang, Liuping Zhang
Many clinical characteristics could also be used to explain the observation of PM deficits among HD patients. First, PM deficits may be related to the high percentage of cerebral atrophy (CA) found in HD patients [32]. Tenkku M et al. [33] demonstrated that patients with central cerebral atrophy had poor memory performance. An alternative explanation may be related to the fact that conventional hemodialysis can cause recurrent acute cerebral ischemia [27]. Mark et al. showed that patients undergoing hemodialysis experience transient declines in cerebral blood flow, correlating with intradialytic cognitive dysfunction [34], which in turn may contribute to a chronic decline in PM function. Additionally, small-vessel cerebrovascular disease is the most common cause of vascular dementia [35]. HD patients often have a series of recognized accelerators of vascular damage risk factors, including hyperlipidemia, hypertension, and an elevated inflammatory state. Finally, the accumulation of various uremic toxins caused by renal failure [36], which plays an important role in the etiology of uremic encephalopathy, might be responsible for the impairment of PM.