Scientists have identified a new avenue of cell death in Alzheimer’s. Scientists the Oregon Health & Sceince University reveals for the first time that a form of cell death known as Ferroptosis — caused by a buildup of iron in cells — destroys microglia cells, a type of cell involved in the brain’s immune response, in cases of Alzheimer’s and vascular dementia.
Also note that the Stanford Scientists Discover Common Genetic Factor That Fends Off Alzheimer’s and Parkinson’s. A large-scale analysis of medical and genetic information revealed that individuals carrying a specific variant of a gene linked to immune function had a reduced risk of developing Alzheimer’s.
They found that the DR4 allelle offers protection.
DR4 is one among copious alleles of a gene called DRB1, which itself is one among many in a large complex of genes — called the human lymphocyte antigen complex, or HLA — that’s crucial to rendering cells’ inner contents visible to the immune system.
A cell’s outer membrane keeps the cell’s insides in and its outsides out. But that’s not all it does. It also serves as a display window, exposing fragments of the proteins inside it to the immune system.
Routine exposure of these fragments, or peptides — stand-alone snippets of chopped-up proteins — on the cell’s surface (its outer membrane) allows roving immune cells to peruse them. By inspecting cell-surface peptides, these patrolling immune cells can see if there’s anything funny going on inside — namely, whether any foreign or altered protein might reside in the cell, implying an infection or cancerous state, respectively.
Facilitating this window shopping are specialized proteins that can grab onto and encase all these peptides and display them on cell surfaces in a way that’s optimal for immune recognition. These specialized proteins are the products of the HLA genes.
Each of the numerous HLA genes comes in a vast variety of alleles. Each of us inherits a different collection of these alleles. Because different HLA alleles’ protein products bind to different sets of peptides, the assortment of peptides a person’s cells display for immune surveillance varies from one person to the next.
When the immune system spots a surface peptide it thinks it’s never seen before, it can mount a powerful attack on any cell displaying that peptide on their surface. Now and then, the judgment turns out to be a case of mistaken identity. Autoimmunity is such a phenomenon.
DR4 is involved in what has been called “protective autoimmunity”: A certain peptide that DR4 knows how to grab onto and display is actually a chemically modified segment of a normal protein our cells make — tau. It’s the chemical modification that’s causing trouble.
Also note that the Stanford Scientists Discover Common Genetic Factor That Fends Off Alzheimer’s and Parkinson’s. A large-scale analysis of medical and genetic information revealed that individuals carrying a specific variant of a gene linked to immune function had a reduced risk of developing Alzheimer’s.
They found that the DR4 allelle offers protection.
DR4 is one among copious alleles of a gene called DRB1, which itself is one among many in a large complex of genes — called the human lymphocyte antigen complex, or HLA — that’s crucial to rendering cells’ inner contents visible to the immune system.
A cell’s outer membrane keeps the cell’s insides in and its outsides out. But that’s not all it does. It also serves as a display window, exposing fragments of the proteins inside it to the immune system.
Routine exposure of these fragments, or peptides — stand-alone snippets of chopped-up proteins — on the cell’s surface (its outer membrane) allows roving immune cells to peruse them. By inspecting cell-surface peptides, these patrolling immune cells can see if there’s anything funny going on inside — namely, whether any foreign or altered protein might reside in the cell, implying an infection or cancerous state, respectively.
Facilitating this window shopping are specialized proteins that can grab onto and encase all these peptides and display them on cell surfaces in a way that’s optimal for immune recognition. These specialized proteins are the products of the HLA genes.
Each of the numerous HLA genes comes in a vast variety of alleles. Each of us inherits a different collection of these alleles. Because different HLA alleles’ protein products bind to different sets of peptides, the assortment of peptides a person’s cells display for immune surveillance varies from one person to the next.
When the immune system spots a surface peptide it thinks it’s never seen before, it can mount a powerful attack on any cell displaying that peptide on their surface. Now and then, the judgment turns out to be a case of mistaken identity. Autoimmunity is such a phenomenon.
DR4 is involved in what has been called “protective autoimmunity”: A certain peptide that DR4 knows how to grab onto and display is actually a chemically modified segment of a normal protein our cells make — tau. It’s the chemical modification that’s causing trouble.
