[Neurotrophin-associated mechanisms of delayed-onset muscle soreness: research progress and perspective].

Delayed-onset muscle soreness (DOMS) is a common phenomenon that occurs following a sudden increase in exercise intensity or unfamiliar exercise, significantly affecting athletic performance and efficacy in athletes and fitness individuals. DOMS is characterized by allodynia and hyperalgesia, and their mechanisms remain unclear. Recent studies have reported that neurotrophic factors, such as nerve growth factor (NGF) and glial cell derived neurotrophic factor (GDNF), are involved in the development and maintenance of DOMS. This article provides a review of the research progress on the signaling pathways related to the involvement of NGF and GDNF in DOMS, hoping to provide novel insights into the mechanisms underlying allodynia and hyperalgesia in DOMS, as well as potential targeted treatment.

Atopic dermatitis: allergic dermatitis or neuroimmune dermatitis?

Abstract: Advances in knowledge of neurocellulars relations have provided new directions in the understanding and treatment of numerous conditions, including atopic dermatitis. It is known that emotional, physical, chemical or biological stimuli can generate more accentuated responses in atopic patients than in non-atopic individuals; however, the complex network of control covered by these influences, especially by neuropeptides and neurotrophins, and their genetic relations, still keep secrets to be revealed. Itching and airway hyperresponsiveness, the main aspects of atopy, are associated with disruption of the neurosensory network activity. Increased epidermal innervation and production of neurotrophins, neuropeptides, cytokines and proteases, in addition to their relations with the sensory receptors in an epidermis with poor lipid mantle, are the aspects currently covered for understanding atopic dermatitis.

La inflamación neurogénica en la psoriasis: una nueva hipótesis fisiopatológica / Neurogenic inflamation in psoriaris: a new physiopathological hypothesis

La psoriasis es un trastorno dermatológico inflamatoriocrónico. Se cree que es un proceso auto inmune. Diferentesinvestigaciones recientes sitúan a la inflamaciónneurogénica, un proceso proliferativo de fibras nerviosasno mielinizadas, como uno de los factores etiopatogénicoscomunes en la proliferación y mantenimiento de la placapsoriasica. El NGF (Factor de crecimiento Nervioso), unamolécula de la familia de las neurotrofinas, podría ser eliniciador, y perpetuar la señalización celular, mediantesegundos mensajeros, como los neuropéptidos(Substáncia P, Péptido del gen relacionado con lacalcitonina y Péptido Intestinal Vasoacitivo), de dichoproceso inflamatorio, lo que explicaría fenómenos comoel de Koebner o la simetría de las lesiones, en la Psoriasis.Por dicha razón, se comienza a observar a la enfermedad,como un proceso psicosomático. El cerebro generaríaseñalizaciones neuroquímicas, que modularían elproceso periférico, y viceversa. Se explicaría porqué elestrés es el factor de riesgo principal en la psoriasis. Laenfermedad mental, que produce estrés neuronal, pormedio de mecanismos neurobiológicos, podría generar,en el nervio periférico, mecanismos anti-apoptoticos, enpersonas genéticamente vulnerables. Se explicaría tambiénque la misma psoriasis produjera estrés psicosocial,por lo que se cerraría el círculo fisiopatologico

Psoriasis is a cronic inflamatory dermatologic disease.Scientific works believe that is an auto-inmune disease.Novel investigations describe Neurogenic Inflammation,a proliferative process into the unmielinized nervous fibers,like one of the most important common etiopathogenicfactor in the proliferation and maintenance of the psoriaticplaque. The Neural Grow Factor, a molecule of theneurotrophine familily, probably can act like aninicialization and maintenance of the molecular cellularsignaling, with the contribution of other second messengers(Substance P, Calcitonin-gene related peptide andVasoactive Intestinal Peptide), of the inflammatory process,that explain the Koebener phenomenon or the simmetryof the lesions of Psoriasis. For this reason, the disease is actually observed like a psicosomatic illnes. The brain,probably generates neurochemical signaling, thatmodulate the periferical process, and viceversa. Thisexplains the stress like the most important risk factor inthe development of Psoriasis. The mental disease, thatproduce neuronal stress, with neurobiologicalmechanims, probably generates, in the periferal nerve,antiapoptotic mechanims, in genetically vulnerablepatients. This explains, in the other hand, that psoriasisgenerates psicosocial stress, and close the vicious circleof the etiopathogenic mechanisms of Psoriasis