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ALL ARTICLES AND PRODUCT INFORMATION PROVIDED ON THIS WEBSITE ARE FOR INFORMATIONAL AND EDUCATIONAL PURPOSES ONLY. The products offered on this website are furnished for in-vitro studies only. In-vitro studies (Latin: in glass) are performed outside of the body. These products are not medicines or drugs and have not been approved by the FDA to prevent, treat or cure any medical condition, ailment or disease. Bodily introduction of any kind into humans or animals is strictly forbidden by law.

Buntanetap: A Promising Small Molecule Inhibitor for Neurodegenerative Diseases

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Figure 2. The role of TDP-43 in neurodegeneration of motor neurons

Buntanetap has been demonstrated to be a multitargeted therapy capable of decreasing neurotoxic proteins involved in the development and progression of AD by reducing the levels of amyloid beta, improving neuroplasticity, and reducing neuroinflammatory species. Moreover, this novel therapy can also decrease PD-related proteins like alpha-synuclein and TDP-43, which have been demonstrated to have a role in the degeneration of motor neurons, thus causing the progression of neurodegenerative disorders like PD. In general terms, Buntanetap promotes the recovery of cognition, increases proliferation, improves neuronal plasticity, and significantly reduces neuroinflammation, thus slowing down the progression of PD and AD.[2,3,5]

miRNA Researched for Parkinson's Disease: Neuroprotection Blocks Neuron Death

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Programmed cell death, better known as apoptosis, is crucial in eliminating abnormal or unwanted cells in the body.[2] In recent years, the complex pathways regulating apoptosis have been well-studied as potential therapy targets.[2,10] Parkinson's disease (PD) is no exception since the leading cause of this disorder is the death of dopamine-producing neurons in the brain (see Fig.1).[1-4] PD is a debilitating neurodegenerative disorder that steals a person's ability to control movement.[8] Currently, levodopa (L-Dopa) is the most effective treatment for PD, helping in the improvement of the symptoms but not in the progression of the disease.[3] In addition, the use of L-Dopa led to adverse reactions after long-term administration.[3,7] Several studies propose using microRNAs (miRNAs) to inhibit the apoptosis of the dopamine-producing neurons found in PD.[6-9] miRNAs are tiny molecules capable of regulating gene expression (molecular switches) in the most critical processes for cell survival, like proliferation, cell differentiation, and apoptosis when required.[5-8]

Figure 1. The comparison between the normal functioning of dopaminergic neurons in healthy individuals vs in PD patients. 

Dopamine Neurons Parkinson's

For this reason, understanding the role of miRNAs in PD could be vital to developing new treatments to decrease the progression of the disorder. The apoptosis process is significant for eliminating unwanted cells.[2] Therefore, using miRNAs as a therapy has the potential to inhibit unwanted cell death and induce apoptosis in abnormal cells as well.[3-6] Understanding this interplay between miRNAs and apoptosis could lead to new treatment strategies for PD.[7] Several investigations found that miRNAs have neuroprotection abilities, safeguarding neurons from apoptotic cell death.[5] Alternatively, miRNAs promote apoptosis, thus eliminating damaged or dysfunctional neurons, which is crucial to clear cellular debris from microenvironments.[5]

Some benefits of using miRNAs as a therapy for PD are the following: (1) miRNAs can target specific genes involved directly in the apoptotic pathway (specificity). (2) miRNAs are molecular switches, activating or inhibiting the apoptosis pathway. This adaptive characteristic is very convenient for this type of therapy since PD requires, in some cases, the inhibition of neuronal death (dopamine-producing neurons) and the activation of apoptosis in unwanted cells in the brain. (3) miRNAs can cross the blood-brain barrier and enter into cells, which is a challenge in developing neurodegenerative diseases. The apoptosis pathway accelerates the progression of PD by the direct dopamine depletion caused by the death of dopamine-producing neurons.[4-6] As the disease progresses, more and more neurons are lost, leading to worsening symptoms and disability.

Lipid Nanoparticles Deliver RNA to the Brain for Alzheimer's

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The inhibition of PU.1 using RNA therapy delivered with lipid nanoparticles as a novel treatment for Alzheimer’s disease.

Neurodegenerative disorders are typically linked to chronic neuroinflammation. Alzheimer’s disease (AD) is not an exception since chronic inflammation is one of the hallmarks that contributes to the progression of the disorder.[2] Microglia cells are the main characters in promoting neuroinflammation since they are the most abundant brain immune cells. [2-5] Microglia cells are well known to clear different waste materials from the brain and confer neuroprotection (see Fig.1).[6] However, recent studies have pointed to the presence of AD-risk locus in the microglia genome.[2] AD-risk loci are specific fragments located in the genome that can potentially promote AD development.[3,14] These AD-risk loci open many opportunities for RNA therapeutic methods.[3,6] RNA therapies have been studied for almost all types of disorders, like Parkinson’s disease, AD, and cancer, among others.[3,9,10] The problem with this type of therapy is that it is difficult to find the correct method for transfection, depending on the area or interest. The transfection process, which introduces RNA into cells, is used to modify the host cell genome, changing the cell fate. [10,11] In the case of inhibiting with RNA transfection therapy, the siRNA is used. [2,12] siRNA (small interfering RNA) are small fragments of artificially synthesized RNA capable of inhibiting a specific genome fragment.[10]

Figure 1. Show the roles of the microglia in a healthy brain versus one with Alzheimer’s disease.[6]

Microglia Alzheimer's

What is JNJ-2113 and How Does it Work?

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About Psoriasis

 In America, psoriasis affects over 8 million people, representing a significant portion of the population. While there is no cure, many people with psoriasis can manage their symptoms effectively with medical treatment and lifestyle adjustments.

Types of Psoriasis

Psoriasis is a chronic autoimmune condition that primarily affects the skin, characterized by the rapid buildup of skin cells leading to thick, red, scaly patches that are often itchy or painful. This acceleration of skin cell growth is due to an overactive immune response. There are several forms of psoriasis, with plaque psoriasis being the most common, marked by raised, inflamed, red lesions covered with a silvery white buildup of dead skin cells. Other forms include guttate psoriasis, which appears as small, dot-like lesions; pustular psoriasis, characterized by white pustules surrounded by red skin; inverse psoriasis, which affects skin folds; and erythrodermic psoriasis, a severe form that leads to widespread redness over most of the body.

Treatments for psoriasis vary based on the type and severity of the condition and can include topical treatments, phototherapy, systemic medications, and biologic drugs, which target specific parts of the immune system. The goal of treatment is to reduce inflammation and clear the skin.

JNJ-2133 in Research

Recently, The FRONTIER 2 long-term extension study, presented at the 2024 American Academy of Dermatology Annual Meeting in San Diego, showed that the JNJ-2113 treatment maintains its effectiveness from Week 16 through Week 52, with safety results aligning with those found in the earlier FRONTIER 1 study. Johnson & Johnson revealed initial outcomes from the FRONTIER 2 study, an extension of the Phase 2b FRONTIER 1 trial, which explores the use of JNJ-2113. This unique, targeted oral peptide aims to inhibit the IL-23 receptor, a key player in the activation of pathogenic T-cells associated with moderate-to-severe plaque psoriasis and other IL-23-mediated conditions in dermatology, rheumatology, and gastroenterology.

Throughout the year-long FRONTIER 2 study, adults with moderate-to-severe plaque psoriasis experienced significant and sustained skin clearance. Across five different dosage groups of JNJ-2113, measured by the Psoriasis Area and Severity Index, the effectiveness of the treatment was consistently upheld from Week 16 to Week 52. Notably, the 100 mg twice-daily group showed the highest skin clearance rates, with a 78.6% response at 16 weeks and a 76.2% response at 52 weeks. Similarly, for key secondary goals like PASI 90, PASI 100, and Investigator's Global Assessment scores, effectiveness was maintained up to Week 52 for all dosage groups.

Overall Study Design JNJ-77242113

The Role of Senescent Cells in Alzheimer's Disease

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The Role of Senescent cells in Alzheimer's Disease

The aging process is strongly associated with developing diseases, such as cardiovascular conditions, hypertension, cancer, diabetes mellitus, osteoporosis, and neurodegenerative diseases, among others. [10,12] Alzheimer's disease (AD) is no exception since aging is a risk factor for late-onset AD (more than 95% of AD cases). [14,15] Another factor highly associated with aging is the increased cellular senescence population of different cell types as we approach older ages (see Fig. 3).[14] Several studies suggest cellular senescence is critical in aging and connected conditions like AD.[2,5,10] Recent investigations have pointed out that senescent cells promote the pathogenesis of AD.[3-6] But what are senescent cells? Senescent cells' particular feature is stopping the proliferation by entering a cell cycle arrest. [12-15] these senescent cells are also known to develop apoptosis resistance and secrete proinflammatory molecules.[11] Senescent cells not only remain even though they are "damaged" but also liberate various chemicals that can initiate inflammation.[3,7] Cellular senescence emerges when a cell receives considerable stress, driving it to "reprogram" its fate to an unlimited cell cycle arrest.[7,9] DNA damage, oncogene triggering, mitochondrial dysfunction, and the accumulation of proteins like the tau and the amyloid beta (Aβ) are well known to initiate senescence in different types of cells (see Fig. 1).[2,12,14]

Figure 1. The comparison between a healthy brain and an AD brain with senescent cells.[14]

Alzheimer's Brain Senescence

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