PSEN1: A Potential Drug Target and Biomarker for Alzheimer's Disease

Target Name: PSEN1

NCBI ID: G5663

PSEN1

PSEN1: A Potential Drug Target and Biomarker for Alzheimer's Disease

Introduction

Alzheimer's disease is a progressive neurodegenerative disorder that affects millions of people worldwide, leading to a significant impact on patients' quality of life, independence, and overall wellbeing. The most common cause of Alzheimer's disease is the neurotransmitter acetylcholine, which is a vital molecule in the brain that plays a crucial role in memory, learning, and movement. However, as the disease progresses, the levels of acetylcholine in the brain decrease, leading to a build-up of beta-amyloid plaques and neurofibrillary tangles, which cause the misfolding of nerve cells and the production of toxic proteins, leading to the progressive neurodegeneration seen in Alzheimer's disease.

PSEN1, a protein that is expressed in the brain, has been identified as a potential drug target and biomarker for Alzheimer's disease. PSEN1 is a key regulator of the acetylcholine receptor, which is responsible for transmitting the effects of acetylcholine on the brain. By targeting PSEN1, researchers hope to improve the treatment options for Alzheimer's disease and potentially slow down or even reverse the progression of the disease.

PSEN1 and its Functions

PSEN1 is a protein that is expressed in the brain and is involved in the regulation of the acetylcholine receptor, which is responsible for transmitting the effects of acetylcholine on the brain. The acetylcholine receptor is a transmembrane protein that consists of an extracellular domain, a transmembrane domain, and an intracellular domain. The intracellular domain of the acetylcholine receptor is the site where it interacts with PSEN1, leading to the regulation of the receptor's activity.

PSEN1 functions as a negative regulator of the acetylcholine receptor by binding to its intracellular domain and preventing it from activating. This interaction between PSEN1 and the acetylcholine receptor is critical for the regulation of the receptor's activity, and PSEN1 plays a crucial role in maintaining the normal function of the brain.

PSEN1 and Alzheimer's Disease

The levels of PSEN1 in the brain are affected by several factors, including age, gender, and the presence of neurodegenerative diseases, such as Alzheimer's disease. Studies have shown that with age, the levels of PSEN1 in the brain decrease, which is associated with an increased risk of Alzheimer's disease. Additionally, individuals with certain genetic mutations, such as APTIMER, are also at an increased risk of developing Alzheimer's disease due to changes in the levels of PSEN1.

PSEN1 has also been linked to the production of beta-amyloid plaques and neurofibrillary tangles, which are hallmark proteins and structures that are associated with the progressive neurodegeneration seen in Alzheimer's disease. Studies have shown that individuals with Alzheimer's disease have lower levels of PSEN1 in the brain, and that PSEN1 has the potential to be a drug target and biomarker for the disease.

PSEN1 as a Potential Drug Target

PSEN1 has been identified as a potential drug target for Alzheimer's disease due to its involvement in the regulation of the acetylcholine receptor and its association with the production of beta-amyloid plaques and neurofibrillary tangles. By targeting PSEN1, researchers hope to improve the treatment options for Alzheimer's disease and potentially slow down or even reverse the progression of the disease.

One approach to targeting PSEN1 is through the use of small molecules, such as inhibitors of PSEN1, which can reduce the levels of PSEN1 in the brain and improve the levels of acetylcholine, which may help to reduce the production of beta-amyloid plaques and neurofibrillary tangles. Additionally, drugs that target

Protein Name: Presenilin 1

Functions: Catalytic subunit of the gamma-secretase complex, an endoprotease complex that catalyzes the intramembrane cleavage of integral membrane proteins such as Notch receptors and APP (amyloid-beta precursor protein) (PubMed:15274632, PubMed:10545183, PubMed:10593990, PubMed:10206644, PubMed:10899933, PubMed:10811883, PubMed:12679784, PubMed:12740439, PubMed:25043039, PubMed:26280335, PubMed:30598546, PubMed:30630874, PubMed:28269784, PubMed:20460383). Requires the presence of the other members of the gamma-secretase complex for protease activity (PubMed:15274632, PubMed:25043039, PubMed:26280335, PubMed:30598546, PubMed:30630874). Plays a role in Notch and Wnt signaling cascades and regulation of downstream processes via its role in processing key regulatory proteins, and by regulating cytosolic CTNNB1 levels (PubMed:9738936, PubMed:10593990, PubMed:10899933, PubMed:10811883). Stimulates cell-cell adhesion via its interaction with CDH1; this stabilizes the complexes between CDH1 (E-cadherin) and its interaction partners CTNNB1 (beta-catenin), CTNND1 and JUP (gamma-catenin) (PubMed:11953314). Under conditions of apoptosis or calcium influx, cleaves CDH1 (PubMed:11953314). This promotes the disassembly of the complexes between CDH1 and CTNND1, JUP and CTNNB1, increases the pool of cytoplasmic CTNNB1, and thereby negatively regulates Wnt signaling (PubMed:9738936, PubMed:11953314). Required for normal embryonic brain and skeleton development, and for normal angiogenesis (By similarity). Mediates the proteolytic cleavage of EphB2/CTF1 into EphB2/CTF2 (PubMed:17428795, PubMed:28269784). The holoprotein functions as a calcium-leak channel that allows the passive movement of calcium from endoplasmic reticulum to cytosol and is therefore involved in calcium homeostasis (PubMed:25394380, PubMed:16959576). Involved in the regulation of neurite outgrowth (PubMed:15004326, PubMed:20460383). Is a regulator of presynaptic facilitation, spike transmission and synaptic vesicles replenishment in a process that depends on gamma-secretase activity. It acts through the control of SYT7 presynaptic expression (By similarity)

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•   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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