👤 E Maioli

Women face greater vulnerability to dementia and Alzheimer's disease (AD), potentially due to estrogen fluctuations across the lifespan. However, its role in vascular brain health is unclear. We investigated associations between lifelong estrogen exposure-endogenous (reproductive span) and exogenous (oral contraceptives [OC], menopausal hormone therapy [MHT])-and late-life vascular brain injury, AD-related atrophy, and We included 352 cognitively unimpaired 70-years-old women from the Gothenburg H70-1944 Birth Cohort with brain MRI and 5-year follow-up. Reproductive lifespan was calculated as age at menopause or oophorectomy minus age at menarche. OC and MHT use were self-reported. Outcomes included cerebral small vessel disease (SVD), AD-related cortical thickness, and white-matter integrity (fractional anisotropy). Linear and multinomial regression and mixed-effects models were adjusted for confounders and stratified by Extended estrogen exposure throughout life-both endogenous and exogenous-appear to support late-life cerebrovascular health in women, with potential genotype-specific neuroprotective effects. Given the current absence of sex-specific prevention guidelines for cognitive disorders, future research should clarify estrogen's longterm impact on brain health and cognition to inform personalized medicine. Show less

Adipose tissue-derived stem cells (ADSCs) possess multipotent differentiation potential and significant immunomodulatory properties, making them valuable in regenerative medicine. However, their adipogenic differentiation can lead to triglyceride accumulation, chronic inflammation, and metabolic dysfunction. This study evaluated the effects of Radio Electric Asymmetric Conveyer (REAC) technology tissue optimization regenerative adipogenesis reprogramming (TO RGN-AR) on ADSC differentiation, focusing on its ability to preserve stemness, suppress adipogenesis, and promote beneficial phenotypes. REAC TO RGN-AR treatment significantly increased the expression of stemness-related genes (Oct-4, Sox2, and Nanog) while downregulating the expression of adipogenic markers (PPAR-γ, LPL, and ACOT2). Additionally, REAC TO RGN-AR treated cells presented a phenotypic shift toward beige adipocytes, characterized by increased TMEM26 expression and reduced ASC-1 expression. These findings underscore the novelty of using REAC TO RGN-AR to modulate cellular endogenous bioelectrical activity, presenting a noninvasive and operator-independent approach to enhance ADSC-based therapies. This work highlights the potential of this treatment to address metabolic disorders and chronic inflammation while advancing regenerative medicine. Show less

We have recently demonstrated that human alpha-atrial natriuretic peptide (alpha-hANP), an amyloidogenic peptide responsible for isolated atrial amyloidosis, binds to a dimeric form of apo A-I belonging to small high-density lipoproteins (HDL). This binding phenomenon is considered a protective mechanism since it inhibits or strongly reduces the ANP aggregation process. The observation that plasma exhibits at least four times greater amyloid inhibitory activity than HDL prompted us to determine whether small HDL are the only ANP plasma-binding factors. After incubation of whole plasma with labelled ANP, the macromolecular complexes were subjected to two-dimensional gel electrophoresis followed by autoradiography. The results presented here provide novel evidence of additional binding proteins, in addition to apo A-I dimer, able to bind ANP in vitro and to prevent its aggregation. The mass spectrometry analysis of the radioactive spots identified them as albumin, alpha-1 antitrypsin, orosomucoid and apo A-IV-TTR complex. The putative impact of these findings in the amyloidogenic/antiamyloidogenic peptides network is discussed. Show less