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Oxidative stress in vascular dementia and Alzheimer's disease: a common pathology. ​

Literature Information ​

DOI10.3233/JAD-2009-1041
PMID19221412
JournalJournal of Alzheimer's disease : JAD
Impact Factor3.1
JCR QuartileQ2
Publication Year2009
Times Cited120
Keywordsoxidative stress, vascular dementia, Alzheimer's disease, neuronal cell death, vascular pathology
Literature TypeJournal Article, Review
ISSN1387-2877
Pages245-57
Issue17(2)
AuthorsStuart Bennett, Melissa M Grant, Sarah Aldred

TL;DR ​

This review highlights the interconnectedness of Alzheimer's disease and vascular dementia, suggesting they represent two extremes of a single pathological continuum influenced by oxidative stress. The findings indicate that both conditions share a common vascular pathology, with oxidative stress playing a central role, thereby advancing our understanding of dementia's underlying mechanisms and potential therapeutic targets.

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oxidative stress · vascular dementia · Alzheimer's disease · neuronal cell death · vascular pathology

Abstract ​

Alzheimer's disease and vascular dementia are the two most common types of dementia with the former being the most predominant. It is evident that oxidative stress, an environment where pro-oxidant species overwhelm antioxidant species, is involved in the pathogenesis of both forms of dementia. An increased level of reactive oxygen species in the vasculature, reduced nitric oxide bioavailability, and endothelial dysfunction leading to vascular disease is associated with vascular dementia. In Alzheimer's disease, an increased amount of amyloid-beta peptide induces elevated reactive oxygen species production thereby causing neuronal cell death and damage. The recent observation that increased atherosclerotic plaque formation is present in the main artery to the brain in Alzheimer's disease, coupled with the association of vascular risk factors with this disease, suggests a link between these two dementias. This review will argue that Alzheimer's disease and vascular dementia are two extremes of one disease, thus assuming a hypothesis where the clinical conditions referred to as dementia are part of a continuum. We propose that the majority of cases share a vascular pathology and that oxidative stress is central to this common pathology.

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Primary Questions Addressed ​

  1. How do different antioxidant therapies compare in their effectiveness for managing oxidative stress in Alzheimer's disease and vascular dementia?
  2. What specific mechanisms link oxidative stress to the formation of amyloid-beta plaques in Alzheimer's disease?
  3. How might lifestyle interventions, such as diet and exercise, mitigate oxidative stress in patients with vascular dementia?
  4. What role do genetic factors play in the susceptibility to oxidative stress-related damage in Alzheimer's disease and vascular dementia?
  5. How can early detection of oxidative stress markers influence treatment strategies for individuals at risk of developing dementia?

Key Findings ​

Key Insights ​

  1. Research Background and Objectives: The study investigates the roles of oxidative stress in two prevalent forms of dementia: Alzheimer's disease (AD) and vascular dementia (VaD). While AD is the most common type, VaD is significant in its own right, often linked to vascular pathology. The research aims to elucidate the common underlying mechanisms, particularly oxidative stress, that contribute to the pathogenesis of both forms of dementia. By proposing that these conditions may represent different ends of a spectrum, the review seeks to highlight the interconnectedness of AD and VaD.

  2. Main Methods and Findings: The review synthesizes existing literature regarding the involvement of oxidative stress in AD and VaD. It examines the biochemical and physiological processes, including the production of reactive oxygen species (ROS) and the consequent oxidative damage. Key findings indicate that in VaD, elevated ROS levels and reduced nitric oxide availability lead to endothelial dysfunction and vascular disease. In contrast, AD is characterized by the accumulation of amyloid-beta, which not only promotes oxidative stress but also results in neuronal cell death. Furthermore, the review notes an association between increased atherosclerotic plaque in the brain's major arteries and AD, suggesting that vascular risk factors may also exacerbate the pathology of AD.

  3. Core Conclusions: The authors conclude that there is a significant overlap in the pathophysiological mechanisms of AD and VaD, primarily driven by oxidative stress. They propose a unified hypothesis that positions these two dementias as varying manifestations of a single underlying disease process, centered around vascular pathology. This perspective challenges the traditional dichotomy between AD and VaD, suggesting that many dementia cases might be better understood as part of a continuum influenced by oxidative stress.

  4. Research Significance and Impact: The implications of this research are profound for both clinical practice and future research directions. Recognizing the shared pathways of oxidative stress in AD and VaD opens avenues for developing targeted therapeutic strategies that address these common mechanisms rather than treating each type of dementia in isolation. This could lead to more effective prevention and treatment modalities that mitigate oxidative damage, potentially improving patient outcomes. Furthermore, it underscores the necessity of managing vascular risk factors not only for the prevention of cardiovascular diseases but also for reducing the risk of developing dementia, highlighting the critical intersection of cardiovascular health and cognitive function. This integrative approach may transform how dementia is viewed and treated in the future, promoting a more holistic understanding of neurodegenerative diseases.

Literatures Citing This Work ​

  1. GLP-1 receptor stimulation reduces amyloid-beta peptide accumulation and cytotoxicity in cellular and animal models of Alzheimer's disease. - Yazhou Li;Kara B Duffy;Mary Ann Ottinger;Balmiki Ray;Jason A Bailey;Harold W Holloway;David Tweedie;Tracyann Perry;Mark P Mattson;Dimitrios Kapogiannis;Kumar Sambamurti;Debomoy K Lahiri;Nigel H Greig - Journal of Alzheimer's disease : JAD (2010)
  2. Prevention of Alzheimer's disease in high risk groups: statin therapy in subjects with PSEN1 mutations or heterozygosity for apolipoprotein E epsilon 4. - Daniel A Pollen;Stephen Baker;Douglas Hinerfeld;Joan Swearer;Barbara A Evans;James E Evans;Richard Caselli;Ekaterina Rogaeva;Peter St George-Hyslop;Majaz Moonis - Alzheimer's research & therapy (2010)
  3. Stress, exercise, and Alzheimer's disease: a neurovascular pathway. - Daniel A Nation;Suzi Hong;Amy J Jak;Lisa Delano-Wood;Paul J Mills;Mark W Bondi;Joel E Dimsdale - Medical hypotheses (2011)
  4. Amelioration of amyloid β-induced cognitive deficits by Zataria multiflora Boiss. essential oil in a rat model of Alzheimer's disease. - Nahid Majlessi;Samira Choopani;Mohammad Kamalinejad;Zahra Azizi - CNS neuroscience & therapeutics (2012)
  5. Effects of DL-3-n-butylphthalide on vascular dementia and angiogenesis. - Lihong Zhang;Lanhai Lü;W M Chan;Yin Huang;Maria S M Wai;David T Yew - Neurochemical research (2012)
  6. Positive evolutionary selection of an HD motif on Alzheimer precursor protein orthologues suggests a functional role. - István Miklós;Zoltán Zádori - PLoS computational biology (2012)
  7. Vascular cognitive impairment and Alzheimer's disease: role of cerebral hypoperfusion and oxidative stress. - Hyun Ah Kim;Alyson A Miller;Grant R Drummond;Amanda G Thrift;Thiruma V Arumugam;Thanh G Phan;Velandai K Srikanth;Christopher G Sobey - Naunyn-Schmiedeberg's archives of pharmacology (2012)
  8. Mulberry Fruit Extract Protects against Memory Impairment and Hippocampal Damage in Animal Model of Vascular Dementia. - Pratchaya Kaewkaen;Terdthai Tong-Un;Jintanaporn Wattanathorn;Supaporn Muchimapura;Wiroje Kaewrueng;Sathaporn Wongcharoenwanakit - Evidence-based complementary and alternative medicine : eCAM (2012)
  9. Psychopathy, adaptation, and disorder. - Daniel Brian Krupp;Lindsay A Sewall;Martin L Lalumière;Craig Sheriff;Grant T Harris - Frontiers in psychology (2013)
  10. Undifferentiated and differentiated PC12 cells protected by huprines against injury induced by hydrogen peroxide. - Marta Pera;Pelayo Camps;Diego Muñoz-Torrero;Belen Perez;Albert Badia;M Victoria Clos Guillen - PloS one (2013)

... (110 more literatures)

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