Unveiling New Strategies Facilitating the Implementation of Artificial Intelligence in Neuroimaging for the Early Detection of Alzheimer's Disease.

Alzheimer's disease (AD) is a chronic neurodegenerative disorder with a global impact. The past few decades have witnessed significant strides in comprehending the underlying pathophysiological mechanisms and developing diagnostic methodologies for AD, such as neuroimaging approaches. Neuroimaging techniques, including positron emission tomography and magnetic resonance imaging, have revolutionized the field by providing valuable insights into the structural and functional alterations in the brains of individuals with AD. These imaging modalities enable the detection of early biomarkers such as amyloid-ß plaques and tau protein tangles, facilitating early and precise diagnosis. Furthermore, the emerging technologies encompassing blood-based biomarkers and neurochemical profiling exhibit promising results in the identification of specific molecular signatures for AD. The integration of machine learning algorithms and artificial intelligence has enhanced the predictive capacity of these diagnostic tools when analyzing complex datasets. In this review article, we will highlight not only some of the most used diagnostic imaging approaches in neurodegeneration research but focus much more on new tools like artificial intelligence, emphasizing their application in the realm of AD. These advancements hold immense potential for early detection and intervention, thereby paving the way for personalized therapeutic strategies and ultimately augmenting the quality of life for individuals affected by AD.

Clinical Implications of Epigenetic Dysregulation in Perinatal Hypoxic-Ischemic Brain Damage.

Placental and fetal hypoxia caused by perinatal hypoxic-ischemic events are major causes of stillbirth, neonatal morbidity, and long-term neurological sequelae among surviving neonates. Brain hypoxia and associated pathological processes such as excitotoxicity, apoptosis, necrosis, and inflammation, are associated with lasting disruptions in epigenetic control of gene expression contributing to neurological dysfunction. Recent studies have pointed to DNA (de)methylation, histone modifications, and non-coding RNAs as crucial components of hypoxic-ischemic encephalopathy (HIE). The understanding of epigenetic dysregulation in HIE is essential in the development of new clinical interventions for perinatal HIE. Here, we summarize our current understanding of epigenetic mechanisms underlying the molecular pathology of HI brain damage and its clinical implications in terms of new diagnostic, prognostic, and therapeutic tools.

Phosphodiesterase Inhibition as a Therapeutic Target for Brain Ischemia.

Preclinical studies have shown that phosphodiesterase inhibitors (PDE-Is) represent a potential pharmacological strategy for the treatment of brain ischemia sequelea. PDE-Is 3, 4 and 5 have been tested in several brain ischemia models. All the three PDE-Is after acute or chronic treatment decreased the degree of neurodegeneration and most of them improved functional recovery after brain injury by specific cellular and molecular mechanisms mainly involving an anti-inflammatory and/or neuroprotection action. In contrast to the large number of investigations using PDE-Is in experimental brain ischemia research, the number of clinical studies is still limited. The purpose of this review is to summarize the data currently available on the effects of PDE-Is in experimental models of cerebral ischemia.