Osteoarthritis (OA) is a joint condition that causes significant impairment of the chondrocyte. The gradual degradation of the cartilage lining of one or more freely moving joints, as well as persistent inflammation, are the causes of osteoarthritis. Current medications focus on alleviating symptoms rather than curing the condition. The aim of this review is to evaluate the potential use of fibroblast growth factor receptor 1-bound extracellular vesicle as novel therapy for osteoarthritis. This review article was completed by searching for the keywords “Fibroblast Growth Factor Receptor 1”, “Extracellular Vesicle”, and “Osteoarthritis” in various journals in several search engines. Of the 102 scientific articles found, 95 were found suitable to be used as material in the making of this article. The upregulated amount of FGFR1 (fibroblast growth factor receptors) signalling suggesting the progression of degenerative cartilage that commonly seen in osteoarthritis (OA) patients. Several studies showed that the involvement of extracellular vesicles (EV) derived from MSCs could enhance cartilage repair and protect the cartilage from degradation. EVs have the potential to deliver effects to specific cell types through ligand-receptor interactions and several pathway mechanisms related with the FGFR1. EVs and FGFR1-bound Evs have been postulated in recent years as possible therapeutic targets in human articular cartilage. The protective benefits on both chondrocytes and synoviocytes in OA patients can be achieved by administering the MSC-EVs that may also stimulate chondrocyte proliferation and migration EVs have a promising potential to become a novel therapy for treating patients with OA. However, further researches are need to be conducted to discover further the application of this therapy.

Multi-infarct dementia (MID) is described as a chronic progressive decline in cortical cognitive function due to the occurrence of multiple infarcts in the cerebral vascularization throughout the gray and white matter. Current therapies of MID mostly focus only on slowing down MID progression and symptomatic medications. A novel therapy which is able to provide both preventive and curative properties for MID is of high interest. The purpose of this review is to identify the potential of Compound 21 (C21) gelatin nanoparticle through the nose-to-brain route as therapy for MID. C21, an angiotensin II type 2 receptor (AT2R) agonist, has shown to reduce the size of cerebral infarct in rodent models, resulting in the preservation and improvement of overall cognitive function and prevention of secondary neurodegenerative effects. It is also shown that C21 decreases neuronal apoptosis, improves damaged axons, and encourage synapse development. The challenge remains in preventing systemic AT2R activation and increasing its low oral bioavailability which can be overcome through nose-to-brain administration of C21. Nose-to-brain drug delivery of C21 significantly increases drug efficiency and limits C21 exposure in order to specifically target the multiple infarcts located in the cerebral cortex. Adhering C21 onto gelatin nanoparticles may enable longer contact time with the olfactory and the trigeminal nerve endings, increasing the potency of C21. In summary, treatment of C21 gelatin nanoparticle through nose-to-brain delivery shows high potential as therapy for vascular dementia. However, clinical trials must be further studied in order to test the safety and efficacy of C21.

Alzheimer's disease (AD) is a neurodegenerative disease closely related to the accumulation of beta-amyloid (Aβ) plaques. Growth differentiation factor 11 (GDF11) is one of the proteins that play a role in the aggravation of AD. Decreased concentration of GDF11 disrupts regenerative nervous system, blood vessels, and various vital systems. Low levels of GDF11 with age can be overcome with recombinant GDF11 (rGDF11) to rejuvenate the regenerative effect. Based on research results, rGDF11 enhance the proliferation rate of neuronal precursor cells as well as angiogenesis. rGDF11 can replace lost levels of GDF11, overcome astrogliosis and activation of nerve cell microglia. Therapeutic effect of rGDF11 leads to an improved prognosis in AD patients by neurogenesis and angiogenesis. The prospects of rGDF11 in the treatment of AD have great potential for further research in the future.

Epilepsy, a neurological illness, is characterized by recurrent uncontrolled seizures. There are many treatments of options that can be used as the therapy of epilepsy. However, anti-seizure medications as the primary treatment choice for epilepsy show many possible adverse effects and even pharmacoresistance to the therapy. High Mobility Group Box 1 (HMGB1) as an initiator and amplifier of the neuroinflammation is responsible for the onset and progression of epilepsy by overexpressing P-glycoprotein on the blood brain barrier. HMGB1 proteins then activate TLR4 in neurons and astrocytes, in which proinflammatory cytokines are produced. Anti-HMGB1 mAb works by blocking the HMGB1, reducing inflammatory activity in the brain that may affect epileptogenesis. Through the process, anti-HMGB1 mAb reduces the TLR4 activity and other receptors that may involve in promote signal of epilepsy such as RAGE. Several studies have shown that anti-HMGB1 has the potential to inhibit the increase in serum HMGB1 in plasma and brain tissue. Further research is needed to identify the mechanism of the inhibiting of overexpression of P-glycoprotein through anti-HMGB1 mAb.

Pregnancy hypertensive disorder (PHD) is a broad term referring to conditions related to disorders of high blood pressure during pregnancy. Preeclampsia is one of 4 types of PHD characterized by an increase in systolic blood pressure ≤ 140 mmHg with a diastolic pressure ≤ 90 mmHg accompanied by proteinuria of 1+ or more. Complications of PHD include peripartum cardiomyopathy, maternal mortality, pulmonary edema, cerebrovascular accident and renal failure. As consequence, early detection of PHD is crucial in preventing complications. “Preeclampsia”, “microRNA-125b” and “Biomarker” were the keywords applied to scientific online databases, such as ScienceDirect, PubMed, and Researchgate. A total of 46 journals were screened, reviewed and utilized with utmost precision to construct this literature review. Looking at the dangers of preeclampsia on infants and mothers, miRNA-125b has potential to be used as a biomarker of preeclampsia that can occur in the third trimester. The increase in the concentration of miRNA-125b in the first trimester causes inhibition of trophoblast invasion, which is followed by inhibition of KCNA1, GPC1, and SGPL1. All of these proteins play a role in the invasion trophoblast which is also exacerbated by the increase in the concentration of mir-125b. All in all, these symptoms and the increase of mir-125b that appear in the first trimester yield as a promising result as biomarkers of preeclampsia in the third trimester. Keywords: preeclampsia, microRNA-125b, biomarker, SGPL1, maternal, infants.