Atherosclerosis, Hypertension, and Diabetes in Alzheimer’s Disease, Vascular Dementia, and Mixed Dementia: Prevalence and Presentation

Javanshiri, Keivan; Waldö, María Landqvist; Friberg, Niklas; Sjövall, Fredrik; Wickerström, Karin; Haglund, Mattias; Englund, Elisabet

doi:10.3233/jad-180644

Cited by 49 publications

(39 citation statements)

References 68 publications

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“…The findings of this study were compared with a previous study in which the same study design was used [22], concerning subjects with AD, VaD, and MD from 1992-2017.…”

Section: Methodsmentioning

confidence: 97%

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Cardiovascular Disease, Diabetes Mellitus, and Hypertension in Lewy Body Disease: A Comparison with Other Dementia Disorders

Javanshiri

Haglund

Englund

2019

JAD

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Background: Research concerning the potential roles of cardiovascular disease (CaVD) and diabetes mellitus (DM) as risk factors for Lewy body disease (LBD) is limited. These disorders are, however, established risk factors for vascular dementia (VaD) and have been proposed as risk factors for Alzheimer's disease (AD). Objective: The aim of this study was to investigate the prevalence of CaVD and DM in LBD and compare the results with previous findings in cases with AD, VaD, and mixed AD-VaD (MD). Methods: Autopsy reports at the Clinical Department of Pathology in Lund from 2001-2018 were analyzed. All cases with a complete neuropathological diagnosis of LBD were selected, not distinguishing between subjects with clinical Parkinson disease dementia and dementia with Lewy bodies, on the condition of a clinical diagnosis of dementia. Clinical data were retrieved through the patients' medical records and the Swedish National Diabetes Register (NDR) and compared with those of the AD, VaD, and MD cases. Results: In LBD, there was less CaVD, significantly less DM (p = 0.002) and likewise significantly less hypertension (p < 0.001) than in VaD. The results of the LBD group were consistent with the results of the AD group. Conclusion: Our findings of a low prevalence of CaVD and CaVD risk factors in LBD and in AD argue against the association between these risk factors and their contribution to the development of neurodegenerative diseases.

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“…The findings of this study were compared with a previous study in which the same study design was used [22], concerning subjects with AD, VaD, and MD from 1992-2017.…”

Section: Methodsmentioning

confidence: 97%

“…In this study we compared the prevalence of CaVD and CaVD risk factors in neuropathologically confirmed cases of LBD with findings from a previous article [22], in which the same risk factors in neuropathologically confirmed cases of AD, VaD, and mixed AD-VaD (MD) were studied.…”

Section: Introductionmentioning

confidence: 99%

Cardiovascular Disease, Diabetes Mellitus, and Hypertension in Lewy Body Disease: A Comparison with Other Dementia Disorders

Javanshiri

Haglund

Englund

2019

JAD

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“…Environmental pollutants including tobacco, smoke, and pesticides, like deltamethrin and carbofuran, are responsible for disrupting tau function [14]. Head trauma, hypertension, and diabetes mellitus are disease conditions that can lead to AD [15,16]. Genetics play a major role in causing AD.…”

Section: Etiopathological Factorsmentioning

confidence: 99%

“…Pathogenesis gives information about the cause of AD as well as therapeutic targets. Some plausible etiological factors like genetic defects of APP, PSEN1, PSEN2, and APOE4; environmental toxins like metals, pesticides, and insecticides; head injury; smoking; excess alcohol; viral infection through viruses like HHV-6a and HHV 7; and diseases like hypertension, diabetes, and obesity are somewhat responsible for AD hallmarks including amyloid plaques and NFT [5,[14][15][16]. NFT are formed due to hyperphosphorylation of tau protein and its further processing.…”

Section: Neuropathology Of Alzheimer's Disease Associated With Tau Dymentioning

confidence: 99%

Neuroprotective Approach of Anti-Cancer Microtubule Stabilizers Against Tauopathy Associated Dementia: Current Status of Clinical and Preclinical Findings

Duggal

Mehan

2019

ADR

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Neuronal microtubule (MT) tau protein provides cytoskeleton to neuronal cells and plays a vital role including maintenance of cell shape, intracellular transport, and cell division. Tau hyperphosphorylation mediates MT destabilization resulting in axonopathy and neurotransmitter deficit, and ultimately causing Alzheimer's disease (AD), a dementing disorder affecting vast geriatric populations worldwide, characterized by the existence of extracellular amyloid plaques and intracellular neurofibrillary tangles in a hyperphosphorylated state. Pre-clinically, streptozotocin stereotaxically mimics the behavioral and biochemical alterations similar to AD associated with tau pathology resulting in MT assembly defects, which proceed neuropathological cascades. Accessible interventions like cholinesterase inhibitors and NMDA antagonist clinically provides only symptomatic relief. Involvement of microtubule stabilizers (MTS) prevents tauopathy particularly by targeting MT oriented cytoskeleton and promotes polymerization of tubulin protein. Multiple in vitro and in vivo research studies have shown that MTS can hold substantial potential for the treatment of AD-related tauopathy dementias through restoration of tau function and axonal transport. Moreover, anti-cancer taxane derivatives and epothiolones may have potential to ameliorate MT destabilization and prevent the neuronal structural and functional alterations associated with tauopathies. Therefore, this current review strictly focuses on exploration of various clinical and pre-clinical features available for AD to understand the neuropathological mechanisms as well as introduce pharmacological interventions associated with MT stabilization. MTS from diverse natural sources continue to be of value in the treatment of cancer, suggesting that these agents have potential to be of interest in the treatment of AD-related tauopathy dementia in the future.

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“…It is declining the thinking ability [1]. The major etiology in the pathogenesis of VaD is blockage of cerebral blood vessels and/or reduction of regional and global cerebral blood flow [2]. This leads to depriving the brain cells for vital oxygen and energy by rising of free radicals; reduction of endogenous anti-oxidants and their regulatory enzymes [3].…”

Section: Introductionmentioning

confidence: 99%

Recent Advance of Enzyme Targets for the Management of Vascular Dementia

Muthuraman¹,

Rishitha²,

Islam³

2019

Advances in Dementia Research

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The basic understanding of vascular dementia (VaD) and their molecular mechanisms are a too complex phenomenon. VaD associated neurodegeneration and cognitive impairment are due to multiple complications of the neurovascular system. The progress of VaD is due to the central and/or peripheral pathophysiological process of the neurovascular system. There are limited nootropic agents are employed for the treatment of VaD. Moreover, the explored nootropic agents act on multiple targets such as receptors, enzymes, ion channel, free radicals, cytokines, chemokines, and apoptotic proteins. However, the enzyme targets, especially acetylcholinesterase inhibitors played a crucial role in the management of cognitive disorders. The pathogenesis of VaD is involved in the vascular complication and neurodegenerative process. Hence, the enzymatic regulation of neurovascular complication is expected to prevent the VaD. The present chapter attempts to explore the recent advancement of enzyme targets for the management of VaD.

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Atherosclerosis, Hypertension, and Diabetes in Alzheimer’s Disease, Vascular Dementia, and Mixed Dementia: Prevalence and Presentation

Abstract: AD and VaD exhibit such different profiles of organ and vascular damage as well as of hypertension and DM that they clearly point toward different pathogenic origin with low likelihood of shared risk factors.

Cited by 49 publications

References 68 publications

Cardiovascular Disease, Diabetes Mellitus, and Hypertension in Lewy Body Disease: A Comparison with Other Dementia Disorders

Cardiovascular Disease, Diabetes Mellitus, and Hypertension in Lewy Body Disease: A Comparison with Other Dementia Disorders

Neuroprotective Approach of Anti-Cancer Microtubule Stabilizers Against Tauopathy Associated Dementia: Current Status of Clinical and Preclinical Findings

Recent Advance of Enzyme Targets for the Management of Vascular Dementia

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