Aging and cerebrovascular lesions in pure and in mixed neurodegenerative and vascular dementia brains: a neuropathological study

Reuck, Jacques L. De; Maurage, Claude‐Alain; Deramecourt, Vincent; Pasquier, Florence; Cordonnier, Charlotte; Leys, Didier; Bordet, Régis

doi:10.5114/fn.2018.76610

Cited by 73 publications

(34 citation statements)

References 35 publications

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“…The level of serum amyloid growth correlated negatively with the clinical improvement after ischemia-reperfusion brain injury, which in turn reflected the severity of ischemic injury [91] and/or the development of recurrent ischemic stroke [47]. We can conclude that the proteomic and genomic changes associated with Alzheimer's disease contribute to brain ischemia-reperfusion neurodegeneration [72] with the development of the dementia [7,9,13,15,28,29,34,75,81].…”

Section: Discussionmentioning

confidence: 99%

“…Brain injury after ischemia seems to favour the development of ischemic neurodegeneration of the Alzheimer's disease neuropathologic change [1] by neuronal damage and death [54], neuroinflammation [77], accumulation of all parts of the amyloid protein precursor, especially amyloid [46,58], tau protein dysfunction [67,68] and dysregulation of proteins associated with Alzheimer's disease and their genes [30,63,64], changes in the white matter and general brain atrophy with final development of dementia [66,71,75]. Therefore, it is now required to know the mechanisms underlying the progressive development of irreversible effects in the brain after ischemia.…”

Section: Discussionmentioning

confidence: 99%

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Amyloid pathology in the brain after ischemia

Pluta¹,

Ułamek-Kozioł²,

Januszewski³

et al. 2019

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As the population is aging all over the world, the economic burden of ischemic brain injuries is constantly increasing. Human brain ischemia is one of the leading causes of premature death, significant morbidity and physical and mental disabilities, resulting in a lower quality of life and unusually high costs of health and social care. One of the most difficult problems associated with the pathology of the brain after ischemia is progressive dementia observed in people who survived the stroke. More recently, brain ischemia has been shown to elicit Alzheimer's disease neuropathologic change, possibly facilitating the development of dementia due to the amyloidogenic processing of Alzheimer's disease-related amyloid protein precursor into amyloid. The main purpose of this review is to present the development of Alzheimer's disease neuropathologic change in the brain after human and experimental ischemia, with a particular emphasis on proteins and genes involved in the amyloidogenic processing of the amyloid protein precursor to amyloid.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Amyloid pathology in the brain after ischemia

Pluta¹,

Ułamek-Kozioł²,

Januszewski³

et al. 2019

View full text Add to dashboard Cite

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“…In community‐based studies, the percentage of mixed dementia cases is considerably higher 9 . The likelihood of having mixed dementia increases with age and is highest in people age 85 or older 14,15 …”

Section: Overview Of Alzheimer's Diseasementioning

confidence: 99%

“…9 The likelihood of having mixed dementia increases with age and is highest in people age 85 or older. 14,15 F I G U R E 1 Alzheimer's disease (AD) continuum. *MCI is the acronym for mild cognitive impairment.…”

Section: Mixed Pathologiesmentioning

confidence: 99%

2020 Alzheimer's disease facts and figures

2020

Alzheimer's & Dementia

2,038

653

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This article describes the public health impact of Alzheimer's disease (AD), including incidence and prevalence, mortality and morbidity, use and costs of care, and the overall impact on caregivers and society. The Special Report discusses the future challenges of meeting care demands for the growing number of people living with Alzheimer's dementia in the United States with a particular emphasis on primary care. By mid‐century, the number of Americans age 65 and older with Alzheimer's dementia may grow to 13.8 million. This represents a steep increase from the estimated 5.8 million Americans age 65 and older who have Alzheimer's dementia today. Official death certificates recorded 122,019 deaths from AD in 2018, the latest year for which data are available, making Alzheimer's the sixth leading cause of death in the United States and the fifth leading cause of death among Americans age 65 and older. Between 2000 and 2018, deaths resulting from stroke, HIV and heart disease decreased, whereas reported deaths from Alzheimer's increased 146.2%. In 2019, more than 16 million family members and other unpaid caregivers provided an estimated 18.6 billion hours of care to people with Alzheimer's or other dementias. This care is valued at nearly $244 billion, but its costs extend to family caregivers’ increased risk for emotional distress and negative mental and physical health outcomes. Average per‐person Medicare payments for services to beneficiaries age 65 and older with AD or other dementias are more than three times as great as payments for beneficiaries without these conditions, and Medicaid payments are more than 23 times as great. Total payments in 2020 for health care, long‐term care and hospice services for people age 65 and older with dementia are estimated to be $305 billion. As the population of Americans living with Alzheimer's dementia increases, the burden of caring for that population also increases. These challenges are exacerbated by a shortage of dementia care specialists, which places an increasing burden on primary care physicians (PCPs) to provide care for people living with dementia. Many PCPs feel underprepared and inadequately trained to handle dementia care responsibilities effectively. This report includes recommendations for maximizing quality care in the face of the shortage of specialists and training challenges in primary care.

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“…Notch signalling contributes to the regulation of differentiation and proliferation of endogenous neural cells [5]. Notch is a transmembrane protein receptor, which is activated by binding to DSL and also helps in the regulating of neurogenesis [19].…”

Section: Discussionmentioning

confidence: 99%

Zerumbone promotes proliferation of endogenous neural stem cells in vascular dementia by regulating Notch signalling

Sun

et al. 2019

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Introduction: Present investigation determines the effect of zerumbone on the proliferation of stem cells in vascular dementia (VD) rats. Material and methods: Vascular dementia was induced by cerebral ischemia and reperfusion through non-invasive clamp. Rats were treated with zerumbone 50 mg/kg and 100 mg/kg intraperitoneally 30 min for four weeks after the surgery. Cognitive functions are determined by the Morris water maze (MWM) test and neurological function score in VD rats. Moreover mediators of inflammation and parameters of oxidative stress were estimated in the brain tissue homogenate of ischemia-induced vascular dementia rats. The expression of proteins and mRNA expressions were determined by western blot assay and RT-PCR methods. Moreover histopathological changes were observed by H&E staining on the brain tissue of vascular dementia rats. Results: There was a significant reduction in the cognitive function and neurological score in the zerumbone-treated group compared to the VD group of rats. Data of the study reveal that treatment with zerumbone attenuates the altered level of cytokines and markers of oxidative stress parameters in the brain tissue of VD rats. The expression of NICD, Hes-1 and Nestin proteins was significantly (p < 0.01) reduced in the brain tissue of the zerumbone-treated group compared to the VD group of rats. There was a significant reduction in the mRNA expression of Notch-1 and Hes-1 in the brain tissue of the zerumbone-treated group compared to the VD group of rats. Conclusions: This study concludes that treatment with zerumbone protects the neuronal injury and ameliorates the cognitive function by stimulating the proliferation of endogenous neural stem cells. Moreover proliferation of neural stem cells was stimulated in zerumbone-treated rats by regulating the Notch signalling.

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Aging and cerebrovascular lesions in pure and in mixed neurodegenerative and vascular dementia brains: a neuropathological study

Cited by 73 publications

References 35 publications

Amyloid pathology in the brain after ischemia

Amyloid pathology in the brain after ischemia

2020 Alzheimer's disease facts and figures

Zerumbone promotes proliferation of endogenous neural stem cells in vascular dementia by regulating Notch signalling

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