Risk Factors for β-Amyloid Deposition in Healthy Aging

Rodrigue, Karen M.; Rieck, Jenny; Kennedy, James L.; Devous, Michael D.; Diaz‐Arrastia, Ramon; Park, Denise C.

doi:10.1001/jamaneurol.2013.1342

Cited by 220 publications

(164 citation statements)

References 40 publications

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“…there is elevation of diastolic blood pressure) and later development of AD (61,66,82). Hypertension in cognitively normal adults with at least 1 APOE ϵ4 allele was associated with increased binding of the Aβ tracer F18-labelled florbetapir (116). The conventional interpretation is that hypertension increases the risk of developing AD by promoting the accumulation of Aβ.…”

Section: Therapeutic Implicationsmentioning

confidence: 99%

Cerebral Hypoperfusion and the Energy Deficit in Alzheimer's Disease

Love

Miners

2016

Brain Pathology

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Section: Therapeutic Implicationsmentioning

confidence: 99%

Cerebral Hypoperfusion and the Energy Deficit in Alzheimer's Disease

Love

Miners

2016

Brain Pathology

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“…Necroptic studies of patients with AD showed more atherosclerotic lesions in cerebral vessels associated with more amyloid plaques and neurofibrillary tangles [19,20]. Brain of hypertensive patients has increased amyloid plaques and neurofibrillary tangles [21]. Blood β-amyloid (Aβ), involved in the pathogenesis of AD, is elevated in patients with VCI, contributing to vascular dysfunction [22,23].…”

Section: Ad and Htnmentioning

confidence: 99%

Cardiovascular Alterations in Patients with Dementia

2017

JCCR

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Submit Manuscript | http://medcraveonline.com one of the most susceptible being the brain [1]. Hypertension is a major risk factor for vascular cognitive impairment (VCI) and for Alzheimer disease (AD), the most frequent causes of dementia in the elderly [3]. Continuous elevation in blood pressure has progressive effects on the structure and function of cerebral arteries determining adaptive changes like remodeling, aiming to decrease the mechanical stress on the arterial wall [4]. Remodeling could be hypertrophic or eutrophic and reduces the vesselsˈ lumen increasing the vascular resistance and represents a potential risk factor for cardiovascular and cerebrovascular disease [5].Old hypertension also induces an increase in the stiffness of large arteries which is a good predictor of cognitive decline and stroke and is associated with silent brain lesions [3,6]. HTN is a major risk factor for atherosclerosis. Increase in BP increases the odds of complex aortic atherosclerosis, predictive of ischemic strokes [7]. Atherosclerotic lesions are localised at the site of turbulence of the flow like the carotid bifurcation and the vertebrobasilar system and less frequently in intracranial arteries. Stroke can be produced by releasing fragments from atherosclerotic plaques (artery-to-artery embolism) or by rupture and hemorrhage with acute cerebrovascular occlusions.HTN also provokes small vessel disease (SVD) in which the most frequent pathological substrate is arteriolosclerosis [8], affecting the deep hemispheric white matter and basal ganglia. One of the pathological features of arteriosclerosis is lipohyalinosis [8] and in advanced lesions rupture of the vessel with microscopic or macroscopic hemorrhages disposed typically in basal ganglia or thalamus. Capillary rarefaction induces lesions in the periventricular white matter. Brain alterations underlying VCIVCI includes a spectrum of cognitive alterations due to cerebrovascular factors, ranging from mild to full blown vascular dementia impairing the daily lifeˈs activities [3]. A major cause of cognitive impairment is stroke. Having a stroke doubles the risk of dementia (poststroke dementia) [3]. The risk of VCI is incresed in patients with no history of stroke but with brain infarcts (silent infarcts) at imagistic investigations. Strategic-infarct dementia is produced by a single stroke affecting a region important for cognition like the frontal lobe or the thalamus [3]. Multi-infarct dementia can also results from multiple strokes destroying large amounts of brain tissue [3]. SVD is a major cause of VCI, being responsible for up to 45 % of dementia cases [3]. Neuropathological alterations caused by cerebral SVD linked with VCILacunar infarcts: Are rounded, < 20 mm diameter lesions, founded more frequently in the basal ganglia, associated with SVD and a strong predictor of VCI [11]. They are caused by acute occlusion of small perforating cerebral arteries or embolism from upstream vessels [12]. Recent studies show the possibility that blood-brain barrier (BBB) alte...

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“…A study of adults possessing at least one ApoE4 allele revealed that hypertensive individuals tended to have significantly higher Aβ burdens than those with normal blood pressure (Rodrigue et al, 2013). Moreover, cholesterol is involved in generation and deposition of Aβ in the brain, though cholesterol modification Among AChEIs, phenserine, ispronicline and ABT-089 have been tested in patients with AD, but resulted in no significant change in cognitive function (Klein, 2007;Becker and Greig, 2012;NIH, 2011).…”

Section: Modifiable Lifestyle Factors In Admentioning

confidence: 99%