Our objective was to evaluate immediate acute changes in myocardial function during the autonomic storm of brain death (BD). Wistar rats were divided into four groups (n = 8/group): controls without any treatment, β-blocker (Esmolol®, 10 mg/kg), calcium channel blocker (Diltiazem®, 10 mg/kg), or alpha-blocker (Prazosin®, 0.3 mg/kg). Treatments were administered intravenously 5 min before BD induction. Echocardiography (ATL-5000, 8 MHz) was performed to measure left ventricular (LV) dimensions and fractional shortening at baseline, during BD induction and 5 min and 15 min after BD. In controls, BD was immediately associated with an increase in wall thickness and a decrease in LV cavity dimension. This myocardial wall hypertrophy was completely prevented by β-blockers, but not with calcium- and alpha-blockers. Extensive myocardial interstitial edema was found in all groups, except in the β-blocker group. Myocardial wall hypertrophy was also prevented during a longer follow-up of 180 min after BD in β-blocker group as opposed to controls. In conclusion, BD is associated with an immediate and severe myocardial damage related to an important interstitial edema which is prevented by β-blockers.
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http://dx.doi.org/10.1111/j.1432-2277.2010.01184.x | DOI Listing |
Ferroptosis, an iron-dependent form of programmed cell death driven by oxidative stress, plays a crucial role in the progression of Alzheimer's disease (AD). Aging diminishes antioxidant systems that maintain iron homeostasis, particularly affecting the glutathione peroxidase (GPX) system, leading to increased ferroptosis and exacerbated neurodegeneration and neuroinflammation in AD. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key transcription factor regulating genes involved in antioxidant defense and ferroptosis.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
College of Public Health, University of Kentucky, Lexington, KY, USA.
Background: Brain arteriolosclerosis (B-ASC) is a pathologic hallmark characterized by dysmorphic brain arteriolar wall thickening. B-ASC is a common finding at autopsy in aged persons - some degree of B-ASC is seen in >80% of brains beyond age 80 years - and is associated with cognitive impairment. Hypertension and diabetes are widely recognized as risk factors for B-ASC.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Rush Alzheimer's Disease Center, Chicago, IL, USA.
Background: The recent approval of two anti-amyloid antibodies, Aducanamab and Lecanamab, have set the stage for the next generation of anti-amyloid treatments. Despite the capability of these treatments to lower Aβ brain levels, there is thus far limited clinical efficacy on cognitive outcomes. Because eligibility for treatment includes individuals with MCI or mild dementia, that often harbor mixed pathologies, the cognitive impact of other brain pathologies may be important.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, Rio De Janeiro, Rio de Janeiro, Brazil.
Background: Alzheimer's disease (AD) is the leading cause of dementia in elderly humans worldwide. More than 40 million people currently suffer from AD, and this prevalence tends to increase considerably in the coming decades due to increased longevity. The unfolded protein response (UPR) is an adaptive signaling mechanism that aims to maintain cell viability under misfolded protein accumulation and endoplasmic reticulum stress.
View Article and Find Full Text PDFNeuromolecular Med
December 2024
Department of Neurology, Liaocheng People's Hospital and Liaocheng Hospital Affiliated to Shandong First Medical University, Liaocheng, 252000, China.
Alzheimer's disease (AD) is a common progressive neurodegenerative disorder, and the vast majority of cases occur in elderly patients. Recently, the accumulation of Aβ and tau proteins has drawn considerable attention in AD research. This review explores the multifaceted interactions between these proteins and their contribution to the pathological landscape of AD, encompassing synaptic dysfunction, neuroinflammation, and PANoptosis.
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