Hypertension and Dementia

Abstract

Although hypertension is well known as a cause of vascular dementia (VaD), recent findings highlight the role of hypertension in the pathogenesis of Alzheimer's disease (AD) as well as mild cognitive impairment (MCI). Recent studies have shown that disruption of diurnal blood pressure (BP) variation is closely associated with cognitive impairment via injury of the small cerebral arteries indicating that long-standing hypertension constitutes a risk of brain matter atrophy or white matter lesions (WMLs). In several clinical trials, BP-lowering with antihypertensive agents was suggested to reduce the risk of dementia or cognitive decline. This review paper focuses on the role of hypertension as a risk factor for cognitive impairment, and summarizes current knowledge on the relationships between ambulatory BP monitoring (ABPM) and cognitive impairment. Finally, an overview of the impact of antihypertensive therapy on dementia prevention is provided.

Inflammation, Aging and Cancer: Friend or Foe?

“…Aging process is also associated with minor or major changes in immune response profiles and co-expression and co-existence of mismatched or misdirected inflammatory mediators (e.g., TNF-, IL-6, IFN-,, IFNs, PGE2, etc) features that are characteristics of immunoscenescence involved in a wide range of chronic diseases (Davalos et al 2010, Ginaldi et al, 2005, Chung et al, 2008, Khatami 2008, 2011a, Nagai et al, 2010, Ren et al, 2009, Romanyukha and Yashin 2003, Sansoni et al, 2008, Sedivy et al, 2008, Serbina et al, 2008, Siffrin et al, 2007, Zhang 2010 (Figures 3 and 4). Briefly, low grade (unresolved or subclinical) inflammation and longevity are known as comorbidity and co-mortality risk factors in the genesis and progression of nearly all chronic illnesses.…”

“…However, longevity and the rate of functional capacities of organ systems and susceptibility to chronic diseases vary in individuals, due to a combination of genetics, immunological or biological factors and the frequency of exposure to diverse environmental hazards. In an attempt to find a common forum on enormous amount of fragmentary information on the biology of chronic diseases that are linked to inflammation, highlights of major molecular theories of aging are outlined in the following (reviewed in Khatami 2009 (Deng et al, 2008, Ginaldi et al, 2005, Goronzy and Wevand 2005, Khatami 2009a, Nagai et al, 2010, Siffrin et al, 2007, Vasto et al, 2008, Zhang 2010 (Campisi 2011, Chidgev et al, 2007, Chung et al, 2008, Davalos et al, 2010, Deng et al, 2008, Gounaris et al, 2006, Khatami 2008a, Klein et al, 2009, Montavani et al, 2004, O'Brien et al, 2008, Romanyukha and Yashin 2003 (Figures 3 and 4). c. Hormones, Metabolites and Lipids in Biology of Aging: Aging process is associated with altered functions of important hormones (e.g., estrogen, progesterone, insulin, glucagon, androgen, andosterone, testosterone, thyroxine, glucocorticoids, epinephrine, cortisol, mineralcorticoids, dehydroepiandosterone-DHEA, etc) and hormone-like growth factors (e. g., IGF-1, FGF, EGF, VEGF, etc).…”

Inhibition of the Cerebral Renin-Angiotensin System to Limit Cognitive Decline in Elderly Hypertensive Persons

“…Disruption of the normal diurnal BP rhythm is closely associated with cognitive impairment via injury of the small cerebral arteries [15]. Overall, without the BP readings in the various groups understudy, this paper although otherwise compelling, does not conclusively show that the beneficial effect of ARBs or lisinopril on cognitive function is due to inhibition of central cerebral A-II receptors.…”

Cognitive disorders in patients with essential hypertension and their treatment

“…Доказано, что АГ повышает риск развития не только инсульта, но и расстройств памяти и других когнитивных (познавательных) функций, приводя к развитию умеренных когнитивных нарушений и деменции [4,5].…”

“…Сочетанная болезнь Альцгеймера -АГ рассматривается как фактор, ускоряющий реализацию генетической пред-расположенности к этому дегенеративному заболеванию [5,7,18]. АГ вызывает сужение церебральных артерий, патоло-гические изменения в веществе головного мозга (лейкоаре-оз, «немые» лакунарные инфаркты, клинически явные ин-сульты), которые в свою очередь уменьшают церебральную перфузию, способствуя дегенеративным процессам в голов-ном мозге (образование β-амилоида, τ-протеина), характер-ным для болезни Альцгеймера.…”