Association between lower limb strength, anxiety, and depression symptoms in older adults.

The central and peripheral nervous systems constitute a highly organized, dynamic, and complex network of neurons and glial cells that coordinate electrical and chemical signaling to enable information processing, regulation of physiological responses, and maintenance of systemic homeostasis (). The integrity of this system depends on the preservation of membrane architecture, cytoskeletal stability, tightly regulated synaptic transmission, and finely tuned intracellular signaling cascades (; ). Disruption at either the molecular or network level may lead to a broad spectrum of neurological disorders, ranging from acute neuromuscular paralysis and synaptopathies to progressive neurodegenerative conditions, including motor neuron degeneration and cognitive impairment (; ). Among the diverse factors capable of perturbing neural function, infectious agents occupy a distinctive position. Pathogenic bacteria mediate their pathogenic effects not only through direct tissue invasion but also through the secretion of highly specific exotoxins that target and reprogram essential host cellular pathways (; ). These toxins alter the intracellular environment by mechanisms such as inhibition of protein synthesis, cytoskeletal disruption, modulation of membrane permeability, and interference with vesicular trafficking, thereby facilitating bacterial survival and disease progression (). Bacterial neurotoxins represent a specialized subset of these exotoxins that selectively target critical neuronal structures and processes. These molecules typically bind to neuronal receptors with high specificity, undergo internalization, and interfere with essential components of synaptic transmission. The consequences include impaired neurotransmitter release, altered neuronal excitability, or functional synaptic paralysis. Initially regarded solely as virulence factors, these molecules exhibit remarkable specificity that reflects highly evolved host-pathogen molecular interactions (; ).