Chronic Traumatic Encephalopathy and Neuropathological Comorbidities

Stein, Thor D.; Crary, John F.

doi:10.1055/s-0040-1713628

Cited by 12 publications

(7 citation statements)

References 126 publications

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“…For example, cardiovascular risk factors are strongly correlated with sporadic AD ( Leszek et al, 2020 ). Another significant risk factor for sporadic AD is TBI, especially chronic traumatic encephalopathy ( Van Den Heuvel et al, 2007 ; Stein and Crary, 2020 ). AD is characterized by decreased blood flow in the brain and dysfunction of the neurovascular unit, which likely causes impaired oxygenation ( Ahmad et al, 2020 ; Yu et al, 2020 ).…”

Section: Role Of Hif-1α In Neurodegenerative Diseasesmentioning

confidence: 99%

Hypoxia-Inducible Factor (HIF) in Ischemic Stroke and Neurodegenerative Disease

Митрошина

Savyuk

Ponimaskin

et al. 2021

Front. Cell Dev. Biol.

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Hypoxia is one of the most common pathological conditions, which can be induced by multiple events, including ischemic injury, trauma, inflammation, tumors, etc. The body’s adaptation to hypoxia is a highly important phenomenon in both health and disease. Most cellular responses to hypoxia are associated with a family of transcription factors called hypoxia-inducible factors (HIFs), which induce the expression of a wide range of genes that help cells adapt to a hypoxic environment. Basic mechanisms of adaptation to hypoxia, and particularly HIF functions, have being extensively studied over recent decades, leading to the 2019 Nobel Prize in Physiology or Medicine. Based on their pivotal physiological importance, HIFs are attracting increasing attention as a new potential target for treating a large number of hypoxia-associated diseases. Most of the experimental work related to HIFs has focused on roles in the liver and kidney. However, increasing evidence clearly demonstrates that HIF-based responses represent an universal adaptation mechanism in all tissue types, including the central nervous system (CNS). In the CNS, HIFs are critically involved in the regulation of neurogenesis, nerve cell differentiation, and neuronal apoptosis. In this mini-review, we provide an overview of the complex role of HIF-1 in the adaptation of neurons and glia cells to hypoxia, with a focus on its potential involvement into various neuronal pathologies and on its possible role as a novel therapeutic target.

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Section: Role Of Hif-1α In Neurodegenerative Diseasesmentioning

confidence: 99%

Hypoxia-Inducible Factor (HIF) in Ischemic Stroke and Neurodegenerative Disease

Митрошина

Savyuk

Ponimaskin

et al. 2021

Front. Cell Dev. Biol.

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“…However, the occurrence of multiple pathologies also increases with age, and the studies reviewed here indicate that is also true for CTE cases with an older age at death. The development of comorbid pathology is likely related to age, the severity and amount of exposure to repetitive head injury, and other individual genetic and environmental factors [ 83 ]. With increased global brain banking efforts, there will be an increased frequency of CTE cases with an older age at death and comorbid pathology.…”

Section: Discussionmentioning

confidence: 99%

“…For a detailed description and visualisation of CTE pathological features see reference [ 57 ]. These diagnostic criteria allow for more standardised classification of CTE pathology, but it is widely acknowledged that multiple neuropathologies such as CTE p-tau lesions, beta-amyloid plaques, cerebral amyloid angiopathy, Lewy body disease, and TDP-43 proteinopathy can be present in the brain of a single individual, and that this cooccurrence is more common with increasing age [ 83 ].…”

Section: Introductionmentioning

confidence: 99%

Neuropathology in chronic traumatic encephalopathy: a systematic review of comparative post-mortem histology literature

Murray

Osterman

Bell

et al. 2022

acta neuropathol commun

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Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive head trauma and is characterised by the perivascular accumulation of hyperphosphorylated tau (p-tau) in the depths of cortical sulci. CTE can only be diagnosed postmortem and the cellular mechanisms of disease causation remain to be elucidated. Understanding the full scope of the pathological changes currently identified in CTE is necessary to identify areas requiring further research. This systematic review summarises the current literature on CTE pathology from postmortem human tissue histology studies published until 31 December 2021. Publications were included if they quantitively or qualitatively compared postmortem human tissue pathology in CTE to neuropathologically normal cases or other neurodegenerative diseases such as Alzheimer’s disease (AD). Pathological entities investigated included p-tau, beta-amyloid, TDP-43, Lewy bodies, astrogliosis, microgliosis, axonopathy, vascular dysfunction, and cell stress. Of these pathologies, p-tau was the most frequently investigated, with limited reports on other pathological features such as vascular dysfunction, astrogliosis, and microgliosis. Consistent increases in p-tau, TDP-43, microgliosis, axonopathy, and cell stress were reported in CTE cases compared to neuropathologically normal cases. However, there was no clear consensus on how these pathologies compared to AD. The CTE cases used for these studies were predominantly from the VA-BU-CLF brain bank, with American football and boxing as the most frequent sources of repetitive head injury exposure. Overall, this systematic review highlights gaps in the literature and proposes three priorities for future research including: 1. The need for studies of CTE cases with more diverse head injury exposure profiles to understand the consistency of pathology changes between different populations. 2. The need for more studies that compare CTE with normal ageing and AD to further clarify the pathological signature of CTE for diagnostic purposes and to understand the disease process. 3. Further research on non-aggregate pathologies in CTE, such as vascular dysfunction and neuroinflammation. These are some of the least investigated features of CTE pathology despite being implicated in the acute phase response following traumatic head injury.

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“…Furthermore, dynactin pathology and p50-positive NCIs remained unseen in ALS, FTLD-MND, and HpScl [7]. Recently, multiple neuropathologies have received much attention [27,28]. A study of aged persons revealed that about 80% of participants had comorbid multiple neuropathologies, including TDP-43 pathology, at autopsy [29].…”

Section: Pathology Of Perry Diseasementioning

confidence: 99%

Perry Disease: Bench to Bedside Circulation and a Team Approach

Mishima,

Yuasa-Kawada,

Fujioka

et al. 2024

Biomedicines

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With technological applications, especially in genetic testing, new diseases have been discovered and new disease concepts have been proposed in recent years; however, the pathogenesis and treatment of these rare diseases are not as well established as those of common diseases. To demonstrate the importance of rare disease research, in this paper we focus on our research topic, Perry disease (Perry syndrome). Perry disease is a rare autosomal dominant neurodegenerative disorder clinically characterized by parkinsonism, depression/apathy, weight loss, and respiratory symptoms including central hypoventilation and central sleep apnea. The pathological classification of Perry disease falls under TAR DNA-binding protein 43 (TDP-43) proteinopathies. Patients with Perry disease exhibit DCTN1 mutations, which is the causative gene for the disease; they also show relatively uniform pathological and clinical features. This review summarizes recent findings regarding Perry disease from both basic and clinical perspectives. In addition, we describe technological innovations and outline future challenges and treatment prospects. We discuss the expansion of research from rare diseases to common diseases and the importance of collaboration between clinicians and researchers. Here, we highlight the importance of researching rare diseases as it contributes to a deeper understanding of more common diseases, thereby opening up new avenues for scientific exploration.

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Chronic Traumatic Encephalopathy and Neuropathological Comorbidities

Cited by 12 publications

References 126 publications

Hypoxia-Inducible Factor (HIF) in Ischemic Stroke and Neurodegenerative Disease

Hypoxia-Inducible Factor (HIF) in Ischemic Stroke and Neurodegenerative Disease

Neuropathology in chronic traumatic encephalopathy: a systematic review of comparative post-mortem histology literature

Perry Disease: Bench to Bedside Circulation and a Team Approach

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