Targeting CALD1 for Neurodegeneration (G800)

Target Name: CALD1

NCBI ID: G800

CALD1

Targeting CALD1 for Neurodegeneration

CALD1 (long short-chain alpha-lipoic acid) is a protein that is expressed in various tissues throughout the body, including the brain. It is a lipoic acid-conjugated protein that is involved in a number of cellular processes, including energy metabolism, inflammation, and stress resistance.

Recent studies have identified CALD1 as a potential drug target for a number of diseases, including Alzheimer's disease, Parkinson's disease, and diabetes. Its involvement in these conditions has led to a growing interest in the potential therapeutic benefits of targeting CALD1 with small molecules.

One of the reasons for the interest in targeting CALD1 is its involvement in the production of reactive oxygen species (ROS), which are highly reactive molecules that can damage cellular components and contribute to a number of diseases. ROS can be generated by a variety of cellular processes, including metabolism, exercise, and stress.

In Alzheimer's disease, ROS are thought to contribute to the build-up of beta-amyloid plaques, a hallmark of the disease, which can cause neurodegeneration and dysfunction. In Parkinson's disease, ROS are thought to contribute to the destruction of dopamine-producing neurons, which can lead to motor neuron dysfunction. In both conditions, ROS play a role in the production of reactive oxygen species that can damage cellular components and contribute to the development of neurodegeneration.

Targeting CALD1 with small molecules has the potential to interfere with the production of ROS, which could potentially slow the progression of neurodegeneration in both Alzheimer's disease and Parkinson's disease. This approach is being tested in a number of clinical trials, including those for Alzheimer's disease and Parkinson's disease.

Another reason for the interest in targeting CALD1 is its role in energy metabolism. CALD1 is involved in the production of ATP, which is the primary energy source of the cell. In addition, it is involved in the production of adenosine, which is a regulatory molecule that helps to regulate the production of energy in the body.

The build-up of beta-amyloid plaques in Alzheimer's disease is thought to disrupt the production of ATP by inhibiting the activity of the enzyme PKA, which is involved in the production of ATP. In addition, the build-up of beta-amyloid plaques is thought to disrupt the production of adenosine by inhibiting the activity of the enzyme ADP-ribosyltransferase (ARA), which is involved in the production of adenosine.

Targeting CALD1 with small molecules has the potential to interfere with the production of ATP and adenosine, which could potentially slow the progression of neurodegeneration in Alzheimer's disease. This approach is being tested in a number of clinical trials, including those for Alzheimer's disease.

In addition to its involvement in energy metabolism, CALD1 is also thought to be involved in the production of other molecules that are involved in inflammation and stress resistance. For example, it is involved in the production of pro-inflammatory cytokines, such as TNF-alpha and IL-1, which can contribute to inflammation. It is also involved in the production of anti-inflammatory cytokines, such as IL-10, which can help to counteract the production of pro-inflammatory cytokines.

In addition to its involvement in energy metabolism and inflammation, CALD1 is also thought to be involved in the production of other molecules that are involved in stress resistance. For example, it is involved in the production of cortisol, which is a hormone that is produced in response to stress, and it is also involved in the production of glutathione, which is a protein that is involved in stress response.

The build-up of beta-amyloid plaques in Alzheimer's disease is thought to disrupt

Protein Name: Caldesmon 1

Functions: Actin- and myosin-binding protein implicated in the regulation of actomyosin interactions in smooth muscle and nonmuscle cells (could act as a bridge between myosin and actin filaments). Stimulates actin binding of tropomyosin which increases the stabilization of actin filament structure. In muscle tissues, inhibits the actomyosin ATPase by binding to F-actin. This inhibition is attenuated by calcium-calmodulin and is potentiated by tropomyosin. Interacts with actin, myosin, two molecules of tropomyosin and with calmodulin. Also plays an essential role during cellular mitosis and receptor capping. Involved in Schwann cell migration during peripheral nerve regeneration (By similarity)

The "CALD1 Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about CALD1 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   advantages and risks of development, etc.
The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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