Publications by authors named "D Chutoranski"

Introduction: Saccular intracranial aneurysm (sIA) rupture is a serious cerebrovascular event associated with inflammatory destructive processes leading to gradual weakening of the sIA wall. The aim of the present study was to identify the morphological and histological determinants for low wall strength in unruptured sIAs harvested from autopsy subjects.

Material And Methods: A total of eight single unruptured sIAs were identified and excised with adjacent cerebral arteries during 8 of 184 postmortem examinations.

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The term Western diet (WD) describes the consumption of large amounts of highly processed foods, rich in simple sugars and saturated fats. Long-term WD feeding leads to insulin resistance, postulated as a risk factor for Alzheimer's disease (AD). AD is the main cause of progressive dementia characterized by the deposition of amyloid-β (Aβ) plaques and neurofibrillary tangles consisting of the hyperphosphorylated tau (p-Tau) protein in the brain, starting from the entorhinal cortex and the hippocampus.

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Encephalitis/encephalomyelitis in the course of rheumatoid arthritis (RA) remains a matter of debate. We present a case of a patient with encephalomyelitis associated with RA confirmed with post-mortem neuropathological examination. A 68-year-old woman with a long-standing, seropositive history of RA presented progressive disturbances of consciousness.

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Article Synopsis
  • * The study measured PGRN levels in the serum and urine of individuals with fatal TBI and found elevated PGRN concentrations, along with increased expression of PGRN in brain tissue.
  • * These findings suggest that assays for PGRN could improve understanding and diagnosis of TBI, and could help assess risks for neurodegenerative conditions in non-fatal TBI cases.
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Alzheimer's disease (AD) is an aging-dependent, irreversible neurodegenerative disorder and the most common cause of dementia. The prevailing AD hypothesis points to the central role of altered cleavage of amyloid precursor protein (APP) and formation of toxic amyloid-β (Aβ) deposits in the brain. The lack of efficient AD treatments stems from incomplete knowledge on AD causes and environmental risk factors.

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