The Role of BDNF as a Biomarker in Cognitive and Sensory Neurodegeneration

Abstract

Brain-derived neurotrophic factor (BDNF) has a crucial function in the central nervous system and in sensory structures including olfactory and auditory systems. Many studies have highlighted the protective effects of BDNF in the brain, showing how it can promote neuronal growth and survival and modulate synaptic plasticity. On the other hand, conflicting data about BDNF expression and functions in the cochlear and in olfactory structures have been reported. Several clinical and experimental research studies showed alterations in BDNF levels in neurodegenerative diseases affecting the central and peripheral nervous system, suggesting that BDNF can be a promising biomarker in most neurodegenerative conditions, including Alzheimer’s disease, shearing loss, or olfactory impairment. Here, we summarize current research concerning BDNF functions in brain and in sensory domains (olfaction and hearing), focusing on the effects of the BDNF/TrkB signalling pathway activation in both physiological and pathological conditions. Finally, we review significant studies highlighting the possibility to target BDNF as a biomarker in early diagnosis of sensory and cognitive neurodegeneration, opening new opportunities to develop effective therapeutic strategies aimed to counteract neurodegeneration.

A Compared Study of Eicosapentaenoic Acid and Docosahexaenoic Acid in Improving Seizure-Induced Cognitive Deficiency in a Pentylenetetrazol-Kindling Young Mice Model

“…The NeuN-related neurodegeneration induced by PTZ can be ameliorated through supplementation with DHA and EPA, in which EPA showed superiority ( Figure 4 A). Brain-derived neurotrophic factor (BDNF), is a biomarker of neuronal plasticity and plays a critical role in neuronal development and function [ 19 ]. The protein levels of BDNF obviously declined in the PTZ group compared with that of the Con group, while supplementation with EPA and DHA similarly increased the levels of BDNF ( F = 23.61, p = 0.0003).…”

Eurycomanone from <i>Eurycoma longifolia</i> Jack upregulates neurotrophin-3 gene expression in ‍retinal Müller cells <i>in vitro</i>

“…Neurotrophins, such as NT3 and BDNF, have been extensively studied for their central and peripheral neuroprotective effects. ( 27 , 28 ) However, their clinical application presents challenges owing to their short plasma half-life (1.28 and 0.92 min for NT3 and BDNF, respectively) after intravenous administration. ( 29 ) To overcome these limitations, the potency of adeno-associated virus (AAV) gene therapy to increase intracellular NT3 levels has been explored for several diseases, including sarcopenia, ( 30 ) Charcot-Marie-Tooth disease, ( 31 ) and cochlear synaptopathy.…”

An Interaction between Brain-Derived Neurotrophic Factor and Stress-Related Glucocorticoids in the Pathophysiology of Alzheimer’s Disease

“…The critical involvement of BDNF/TrkBmediated signaling, such as phospholipase Cγ (PLCγ)-, PI3k/Akt-, and ERK-signaling in the neuro-and glio-genesis, as well as in synaptic function, is highlighted [4]. As expected, in addition to experimental research studies, clinical evidence also shows that the alteration in BDNF levels in neurodegenerative diseases can be a promising biomarker in most neurodegenerative conditions and neurodegenerative diseases, including Alzheimer's disease (AD) [5]. Furthermore, it has been demonstrated that apoptotic elements, which are considered responsible for manifestations linked to the pathophysiology of AD, interact with various signaling molecules, including BDNF/TrkB, and downstream signaling pathways [6].…”