Early loss of NA activity and anterograde neurotrophin support may contribute to degeneration of vulnerable neurons in PD and other neurodegenerative disorders.
Although altered availability of BDNF underlies many neurological deficits and neurodegenerative disorders, secretion dynamics of endogenous BDNF are unexplored.
Additionally, extracellular brain-derived neurotrophic factor (BDNF), a neuroprotective growth factor released by astrocytes that has been shown to be decreased extracellularly in neurodegenerative disease, was observed in response to γ-syn treatment.
Previous studies have identified Apolipoprotein E (APOE), Cathepsin D (CTSD), and Brain-Derived Neurotrophic Factor (BDNF) as key players of neurodegenerative pathways with their variants associated with different neurodegenerative diseases.
In the present review, we discuss the use of growth factors such as PDGF-BB, VEGF, BDNF, and the antioxidative enzyme neuroglobin in the protection of astrocytes and neurons during the development of neurodegenerative diseases.
In this review, we propose that variance in BDNF levels is critical in determining the course of cellular pathophysiology and the development of cancer or neurodegenerative disorder.
Neurotrophins, such as brain-derived neurotrophic factor (BDNF), have shown promise as neuroprotective agents, indicating their potential in therapeutic strategies for neurodegenerative disease.
These deficits, coupled with the reliance of BFCNs on neurotrophin transport, may explain their vulnerability to age-related neurodegenerative disorders like AD.
This review focuses on the effect of acute and chronic inflammation on BDNF levels in the most common psychiatric and neurodegenerative disorders and aims to shed some light on the possible biological mechanisms that may influence this effect.
Multiple pre-clinical studies suggest that administration of autophagy enhancers, senolytic drugs, plasma from young blood, drugs that enhance neurogenesis and BDNF are promising approaches to sustain normal health during aging and also to postpone age-related neurodegenerative diseases such as Alzheimer's disease.
Neurotrophin receptor p75 (p75<sup>NTR</sup>) signaling is a key pathological factor contributing to neurobehavioral abnormalities in many neurodegenerative diseases.
Brain-derived neurotrophic factor (BDNF) is a neutrotrophic factor essential for the survival and differentiation of neurons and is considered a key target in the pathophysiology of various neurodegenerative diseases, as for example AD.
Interest in brain-derived neurotrophic factor (BDNF) was greatly enhanced when it was recognized that its expression is reduced in neurodegenerative disorders, especially in Alzheimer's disease (AD).
We postulate that exercise will attenuate cortical atrophy and synaptic loss inherent to neurodegenerative disorders - many of which also exhibit aberrant down-regulation of BDNF.
As consequence recent novel therapeutic drugs for neurodegenerative diseases has led to the development of multi target drugs, that possess selective brain MAO A and B inhibitory moiety, iron chelating and antioxidant activities and the ability to increase brain levels of endogenous neurotrophins, such as BDNF, GDNF VEGF and erythropoietin and induce mitochondrial biogenesis.
The common human Val66Met polymorphism of BDNF has been implicated in the pathophysiology of neuropsychiatric and neurodegenerative disorders, and in the outcome of pro-adaptive and therapeutic treatments.
Therefore, our findings support the notion that BDNF contributes to the pathogenesis of neurodegenerative diseases by suppressing AEP via Akt phosphorylation.
The diverse physiological roles of the neurotrophin family have long prompted exploration of their potential as therapeutic agents for nerve injury and neurodegenerative diseases.