Advances in PET Imaging of Degenerative, Cerebrovascular, and Traumatic Causes of Dementia

Eisenmenger, Laura; Huo, Eugene; Hoffman, John M.; Minoshima, Shinsei; Matesan, Manuela; Lewis, David H.; Lopresti, Brian J.; Mathis, Chester A.; Okonkwo, David O.; Mountz, James M.

doi:10.1053/j.semnuclmed.2015.09.003

Cited by 18 publications

(6 citation statements)

References 398 publications

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“…Advanced imaging modalities are now being used to evaluate the positive benefit of future therapeutics longitudinally (36). Diffusion tensor imaging has also become a valuable tool for the detection of brain structure abnormalities after blast injury (37, 38) In order to continue to improve these imaging modalities; it is imperative that the key secondary injury pathways are well characterized in pre-clinical models.…”

Section: Discussionmentioning

confidence: 99%

A mouse Model of Focal Vascular Injury Induces Astrocyte Reactivity, Tau Oligomers, and Aberrant Behavior

et al. 2017

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Neuropsychiatric symptom development has become more prevalent with 270,000 blast exposures occurring in the past 10 years in the United States. How blast injury leads to neuropsychiatric symptomology is currently unknown. Preclinical models of blast-induced traumatic brain injury have been used to demonstrate blood-brain barrier disruption, degenerative pathophysiology, and behavioral deficits. Vascular injury is a primary effect of neurotrauma that can trigger secondary injury cascades and neurodegeneration. Here we present data from a novel scaled and clinically relevant mouse blast model that was specifically developed to assess the outcome of vascular injury. We look at the biochemical effects and behavioral changes associated with blast injury in young-adult male BALB/c mice. We report that blast exposure causes focal vascular injury in the Somatosensory Barrel Field cortex, which leads to perivascular astrocyte reactivity, as well as acute aberrant behavior. Biochemical analysis revealed that mild blast exposure also invokes tauopathy, neuroinflammation, and oxidative stress. Overall, we propose our model to be used to evaluate focal blood-brain barrier disruption and to discover novel therapies for human neuropsychiatric symptoms.This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/) which permits copy and redistribute the material just in noncommercial usages, provided the original work is properly cited.

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Section: Discussionmentioning

confidence: 99%

A mouse Model of Focal Vascular Injury Induces Astrocyte Reactivity, Tau Oligomers, and Aberrant Behavior

et al. 2017

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“…There have been significant recent advances in detecting and monitoring axonal injury and Aβ deposition in living TBI patients, using imaging techniques typically applied in clinical studies of aging, MCI, and AD: MRI of axonal injury and connectivity (diffuse tensor imaging (DTI) and high definition fiber tractography) (MacDonald et al, 2007, 2011; Presson et al, 2015) as well as amyloid PET (Eisenmenger et al, 2016; Gatson et al, 2016; Hong et al, 2014; Kawai et al, 2013; Mitsis et al, 2014; Scott et al, 2016). Several of these clinical analyses replicate data from histopathology studies.…”

Section: Role Of Aβ and Aging In Primary And Secondary Effects Of mentioning

confidence: 99%

Disordered APP metabolism and neurovasculature in trauma and aging: Combined risks for chronic neurodegenerative disorders

Ikonomović

Abrahamson

2017

Ageing Research Reviews

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Traumatic brain injury (TBI), advanced age, and cerebral vascular disease are factors conferring increased risk for late onset Alzheimer’s disease (AD). These conditions are also related pathologically through multiple interacting mechanisms. The hallmark pathology of AD consists of pathological aggregates of amyloid-β (Aβ) peptides and tau proteins. These molecules are also involved in neuropathology of several other chronic neurodegenerative diseases, and are under intense investigation in the aftermath of TBI as potential contributors to the risk for developing AD and chronic traumatic encephalopathy (CTE). The pathology of TBI is complex and dependent on injury severity, age-at-injury, and length of time between injury and neuropathological evaluation. In addition, the mechanisms influencing pathology and recovery after TBI likely involve genetic/epigenetic factors as well as additional disorders or comorbid states related to age and central and peripheral vascular health. In this regard, dysfunction of the aging neurovascular system could be an important link between TBI and chronic neurodegenerative diseases, either as a precipitating event or related to accumulation of AD-like pathology which is amplified in the context of aging. Thus with advanced age and vascular dysfunction, TBI can trigger self-propagating cycles of neuronal injury, pathological protein aggregation, and synaptic loss resulting in chronic neurodegenerative disease. In this review we discuss evidence supporting TBI and aging as dual, interacting risk factors for AD, and the role of Aβ and cerebral vascular dysfunction in this relationship. Evidence is discussed that Aβ is involved in cyto- and synapto-toxicity after severe TBI, and that its chronic effects are potentiated by aging and impaired cerebral vascular function. From a therapeutic perspective, we emphasize that in the fields of TBI- and aging-related neurodegeneration protective strategies should include preservation of neurovascular function.

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“…Bu nedenle görüntüleme yöntemleri ile elde edilen bilgiler ki bunlara "görüntüleme biyomarkerları" diyebiliriz; demans hastalarının tanı/ayırıcı tanısında giderek daha büyük bir role sahip olmaktadır. Görüntüleme biyomarkerları ayrıca demans patofizyolojisini aydınlatma ve yeni -daha iyi tedavi yöntemleri geliştirebilme açısından da büyük öneme sahiptir (1 …”

Section: Demanstatanıyöntemleriunclassified

Nuclear Medicine Methods in Dementia

Budak¹,

Aydın²

2017

Nts

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Advances in PET Imaging of Degenerative, Cerebrovascular, and Traumatic Causes of Dementia

Cited by 18 publications

References 398 publications

A mouse Model of Focal Vascular Injury Induces Astrocyte Reactivity, Tau Oligomers, and Aberrant Behavior

A mouse Model of Focal Vascular Injury Induces Astrocyte Reactivity, Tau Oligomers, and Aberrant Behavior

Disordered APP metabolism and neurovasculature in trauma and aging: Combined risks for chronic neurodegenerative disorders

Nuclear Medicine Methods in Dementia

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