Recent important research results on Alzheimer's disease!

"This article has compiled a number of important research results to read and share the new achievements of scientists in the field of Alzheimer's disease research to everyone! Photo source: httpss.com/ Mysterious link between Alzheimer's disease and diabetes! In a recent study published in the international journal, scientists from the Ulich Research Center in Germany and others have revealed the molecular association between Alzheimer's disease and diabetes; the accumulation of pathological protein blocks is characterized by a series of diseases such as Alzheimer's disease, Parkinson's disease and diabetesFor the first time in the study, researchers used cryogenic electron microscopy technology to obtain clear images of how a single molecule arranged in a protein chain that constitutes a typical diabetic sediment progenitor fiber structure that is very similar to the structure of the central fibers in Alzheimer's diseaseAbout a year ago, american doctorsUnusual protein deposits found in the pancreas of people with diabetes, which are very similar to those found in the brains of patients with multiple neurodegenerative diseases, are one of the most extensive diseases previously known as adult diabetes, a deposit called islet amyloid protein, which is made up of small protein harnesses called protofibrocyts, which are made up of peptide hormones in the presence of diabetes, and which in the pancreas promotes insulin-producing beta cell dysfunction and even death insulin plays a very important role in helping the body lower blood sugar。 Developing simple molecular formulations for Alzheimer's disease: Sometimes complex problems actually have very simple solutions In a recent study published in the International Journal, scientists from the Korea Institute of Advanced Science and Technology and others have studied an effective redox-based strategy that integrates versatility into simple molecular formulations to help ward off neurodegenerative diseasesIn the article, researchers have developed a simple structure, oxidant-active aromatic molecular formulation that simultaneously targets and regulates multiple pathological factors in complex neurodegenerative diseases such as Alzheimer's disease, one of the most popular neurodegenerative diseases that affect the health of one in ten individuals over the age of 10, and early-onset dementia is increasingly affecting the health of young peopleRevealing the molecular mechanisms of toxic proteins spreading in the brains of Alzheimer's patients: The toxic forms of proteins are often thought to induce the death of neurons in the brains of Alzheimer's patients, a recent study published in the International Journal of scientists from Lund University and others found that the proliferation of toxic proteins in the brains of older adults or the simultaneous occurrence of beta amyloid proteins through connected neurons promotes the diffusion of toxic proteinsIn the article, the researchers revealed the molecular mechanisms by which toxic proteins spread in the human brain; the researchers say that toxic proteins spread across different brain regions through direct neuronal connections, as if infectious diseases spread to other sites through different transport routes; in the body's normal aging process, this spread is limited but in Alzheimer's disease this spread is driven by beta amyloid proteins that lead to widespread neuronal death eventually lead to dementiaDifferent Alzheimer's subtypes may be associated with different protein modifications: A new study reveals a possible biological cause of different rates of progress iass in different patientsThe study, led by researchers at Massachusetts General Hospital in the United States, focused on the findings of a protein found in the brain's neurofibre tangles, a well-known feature of the brain's neurofibre tangles, published in the journalVarious modifications, including phosphorylation, occur during the diseaseThe researchers found that the presence of different forms of phosphorylation could explain why the disease has different effectsDoctors have long known that the clinical manifestations of Alzheimer's disease vary widely between patients, including the age of onset, the rate of memory loss, and other clinical indicatorsIn addition, the higher the pathological level in the brain, the more serious the diseaseHowever, there is no clue as to what causes this difference between patientsRevealing ways to address Alzheimer's blood-brain barrier damage: Neuroscientists at the Massachusetts Institute of Technology's Institute of Learning and Memory, developing a laboratory-designed model, reveal how the most common Alzheimer's risk genes cause amyloid plaques to disrupt the brain's pulsatiator system, and show that they can prevent these damage simply by approving drugs for human useAbout people carry ingons of genetic variants that increase their risk of developing Alzheimer's diseaseAlmost every person with Alzheimer's disease, or even some non-Alzheimer's patients, suffers from the condition that amyloid protein deposits on the walls of blood vessels impair the ability of the blood-brain barrier to transport nutrients properly, remove waste, and prevent the invasion of pathogens and harmful substancesIn a new study published this month in the journal, researchers identified genetic mutations that promote pathology through specific vascular cell types and molecular pathways of calcium-modulating phosphataseStudies have shown that the peripheral cells in the blood vessels of the body of a person carrying a mutant produce too many proteinsCauses amyloid proteins to come together and amyloid proteins are more abundant in Alzheimer's diseaseAt the same time, the activation of the molecular pathways of calcium-modulating neurophosphatase in the diseased weekly cells seems to promote an increase in expressionPhoto Credit: The blood-brain barrier was damaged before Alzheimer's disease! Or the culprit! : Alzheimer's disease is most famous for its misfolded beta amyloid protein (beta) and proteins that are always present in the brainHowever, a growing body of research has realized that changes to beta and perhaps not all of the blood-brain barrier sesame also become markers for early neurodegenerative diseasesThe extent of the damage to the cerebral hemorrhage barrier is related to the degree of cognitive dysfunction a person experiences, but it is not clear what causes the destruction of the cerebral barrierWriting in the journal Moon et al., the main genetic risk factor for Alzheimer's disease is linked to the destruction of the blood-brain barrierThe lipoprotein gene encodes a major lipoprotein in the brainThere are three main variants: , andLike almost all genes, people carry two copies of them that may be the same variant or different variantsPeople who carry one variant with one variant have a significantly increased risk of developing Alzheimer's disease as much as twice as much as those who carry both variants than more common variantsPeople with Alzheimer's who carry it develop symptoms earlier than those who don't carry the mutated gene: Deep analysis! Scientists identify key genetic mutations that can effectively reduce the risk of Alzheimer's disease in the population! : About one-third of people with the symptomatic Alzheimer's disease are currently in the population of about 10,000 Americans with the disease, and even many people with mild cognitive impairment, or mild Alzheimer's, about half of the population who have the symptoms will translate into comprehensive Alzheimer's disease that currently has drugs that can slow the progression of the disease to some extent but do not have a drug that completely blocks the progression of the disease or prolongs the patient's lifespanResearchers don't know if the state protects the body against aging-related neurodegenerative diseases such as Alzheimer's disease; Researchers from Stanford University and others in the study looked for genetic factors that could interact with peers to reduce the risk of Alzheimer's disease, or the heterogeneous state or protection against age-related phenotype changes and cognitive decline, but researchers aren't sure whether they can protect the carrying population The largest proteomics study to date has revealed a mysterious link between glucose metabolite sinnuse and Alzheimer's disease! : Today we still don't fully understand the pathophysiology mechanisms of Alzheimer's disease, and scientists from empirics from empirics, published in the International Journal entitled "The Institute of Medicine and others, have linked glucose metabolism proteins to the biological characteristics of Alzheimer's disease by using quantitative mass spectrometry and co-expression network analysis to date The protein network module can be linked to sugar metabolism as one of the most common modules, which is one of the most relevant modules related to pathology and body cognition at the same time, and the ability to enrich genetic risk factors and small glial cells associated with anti-inflammatory states and astrocyte cell protein markers indicate that the biological functions they represent play a key role in the onset of the disease and the proteins from this module increase in the level of the cerebrospinal fluid in the early stages of disease In this study, the researchers identified disease-specific protein and biological processes that could help develop new types of targeted therapies, as well as a group of proteins that regulate glucose metabolism in the body, and proteins that play protective roles in small glial cells and astrocytes, or are strongly associated with the pathological progression of Alzheimer's disease and the body's cognitive impairment Special immune cells may be able to help effectively fight the onset and progression of Alzheimer's disease: In a recent study published in the international journal, scientists from institutions such as the Center for Neurodegenerative Diseases in Bonn, Germany, have developed a new way to stimulate immune cells in the brain to protect the body from the development of Alzheimer's disease In the article, the researchers identified a special antibody that binds to the brain's immune cells called small glial cells, which stimulates the activity of small glial cells to keep them alive longer, more easily divided and easier to detect abnormal substances in mice that are similar to Alzheimer's disease symptoms, and the researchers say that the infamous plaque, known as plaques, is quickly recognized and degraded as a marker for Alzheimer's disease Inflammation may trigger a deadly cycle of Alzheimer's disease: In a recent study published in the international journal, scientists from the University of Bonn and others found that an immune response in the brain seems to play a key role in the process of Alzheimer's disease, which in some ways may "fuel" and trigger inflammation and, in a sense, perpetuate inflammation and affect the health of the patient." The main feature of Alzheimer's disease is the accumulation of beta amyloid (beta), which forms larger plaquebetas in the brain, like molecules on the surface of certain bacteria; over the past million years, Li organic sefactory has evolved special defense mechanisms to resist certain structures, so its components belonging to the so-called congenital immune system often lead to the absorption and digestion of certain scavenger cells Small glial cells in the brain have been taking on this role but doing so trigger a destructive process that seems to be largely directly related to dementia when special molecular complexes such as inflammatory small bodies are activated in small glial cells after contact with beta, which then they move like the wheels of external carrier enzymes, which activate the immune messenger molecule and induce inflammation by directing additional immune cells to the place of action () More wonderful counts! Stay tuned!