More and more research in recent years has focused on neurogenesis and neuroplasticity. The hippocampus is a key location of adult neurogenesis. Because this part of the brain is regulated by environmental variables, it must be mentioned the therapeutic potential for neurodegenerative illnesses and brain injuries. Furthermore, this information challenges the historical concept of a static brain and tries to demonstrate its flexibility, adaptability, and possibility for regeneration. Those mechanisms which are found in a variety of mammalian species, including humans, are important when it comes to adaptive learning and memory, thus providing insights into cognitive well-being and mental health. The discovery of the brain's dynamic nature represented by new neurons, marks a shift in the field of neurology with far-reaching potentials. This paper highlights the significant potential of adult neurogenesis when it comes to clinical applications such as Alz-heimer’s disease.
Background: Degenerative aortic stenosis (AS) and transthyretin cardiac amyloidosis (ATTR-CM), particularly wild-type ATTR (ATTRwt), are age-associated disorders that frequently converge in elderly patients. Their coexistence may obscure diagnosis, amplify heart-failure burden, and complicate risk stratification before and after aortic valve replacement. Methods: This narrative review was conducted using a structured literature search focused on ATTR-CM, AS, transcatheter aortic valve implantation/replacement (TAVI/TAVR), and nuclear cardiology. Priority was given to cohort studies, systematic reviews, consensus documents, and guideline statements. Main findings: Across observational cohorts and meta-analyses, ATTR-CM is consistently identified in a clinically meaningful minority of older patients with severe AS, especially among those referred for TAVI. Reported prevalence varies with age, referral pathway, diagnostic protocol, and whether equivocal grade 1 uptake is included, but most contemporary TAVI-oriented cohorts place definite ATTR-CM in the high single-digit to mid-teen percentage range. Clinical suspicion should increase in patients with disproportionate left-ventricular wall thickening, low-flow low-gradient AS, restrictive physiology, elevated cardiac biomarkers, conduction disease, atrial fibrillation, or extracardiac ATTR clues such as bilateral carpal tunnel syndrome. Conclusions: Bone-avid tracer scintigraphy with 99mTc-pyrophosphate, 99mTc-3,3-diphosphono-1,2-propanodicarboxylic acid, or 99mTc-hydroxymethylene diphosphonate, interpreted with SPECT or SPECT/CT and combined with mandatory exclusion of a monoclonal protein, enables robust non-biopsy diagnosis of ATTR-CM. In severe AS, nuclear diagnosis should be embedded in a pragmatic, multidisciplinary pathway that identifies patients likely to benefit from valve intervention, ATTR-specific therapy, genetic testing, and tailored follow-up.