With your risk of dementia post stroke will your incompetent? doctor DO NOTHING TO PREVENT THAT OUTCOME?
With your risk of dementia post stroke your doctor and hospital (If competent) need to create this protocol and have dementia prevention protocols on hand.
1. A documented 33% dementia chance post-stroke from an Australian study? May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.`
3. A 20% chance in this research. July 2013.
4. Dementia Risk Doubled in Patients Following Stroke September 2018
Do you prefer your doctor and hospital incompetence NOT KNOWING? OR NOT DOING?
Brain’s Immune Cells Found to Protect Against Alzheimer’s Damage
Summary: Researchers have uncovered how the brain’s immune cells, called microglia, can act as protectors rather than destroyers in Alzheimer’s disease. By lowering the immune regulator PU.1, microglia began expressing lymphoid-like receptors that reduced inflammation and preserved cognitive function in mouse models.
Removing CD28, a key receptor on these protective cells, reversed the benefit—accelerating plaque buildup and neuroinflammation. The discovery of this PU.1–CD28 signaling axis reveals a new immune mechanism in Alzheimer’s and opens the door to targeted microglia-based therapies.
Key Facts
- Protective Microglia: Reducing PU.1 levels activated neuroprotective microglia that limited inflammation and preserved cognition.
- CD28’s Role: Deleting CD28 disrupted this protection, accelerating brain inflammation and plaque formation.
- Therapeutic Potential: The PU.1–CD28 axis offers a promising target for Alzheimer’s immunotherapies.
Source: Max Planck Institute
Using Alzheimer’s mouse models, human cells, and human brain tissue, the researchers demonstrated that lowering PU.1 promotes the expression of lymphoid immunoregulatory receptor proteins on microglia.
Despite being present in small numbers, these neuroprotective microglia exert a brain-wide suppressive impact on inflammation and protect cognitive function and survival in mice.
Deleting CD28 from this small subset of microglia amplified inflammation and accelerated plaque growth, highlighting CD28’s key role in protective microglial activity.
“Microglia are not simply destructive responders in Alzheimer’s disease— they can become the brain’s protectors,” said Anne Schaefer, the senior author of the paper and leader of the project.
“This finding extends our earlier observations on the remarkable plasticity of microglia states and their important roles in diverse brain functions. It also underscores the vital importance of international collaboration in advancing scientific progress.”
“It is remarkable to see that molecules long known to immunologists for their roles in B and T lymphocytes also regulate microglial activity,” added Alexander Tarakhovsky.
“This discovery comes at a time when regulatory T cells have achieved major recognition as master regulators of immunity, highlighting a shared logic of immune regulation across cell types. It also paves the way for immunotherapeutic strategies for Alzheimer’s disease.”
The study builds on pioneering genetic work by Alison Goate, a senior co-author of the study, who identified a common variant in SPI1—the gene encoding PU.1—as being associated with reduced Alzheimer’s risk. “These results provide a mechanistic explanation for why lower PU.1 levels are linked to reduced Alzheimer’s risk,” said Goate.
The discovery of the PU.1–CD28 axis establishes a molecular framework for understanding protective microglial states and highlights the potential of microglia-targeted immunotherapies to modify the course of Alzheimer’s disease.
Key Questions Answered:
A: The study showed that lowering the protein PU.1 activates a small population of microglia that suppress inflammation and protect the brain from Alzheimer’s-related damage.
A: Deleting CD28 from these protective microglia caused inflammation to surge and plaques to grow faster, revealing CD28’s essential role in maintaining brain-protective immune activity.
A: The findings identify a new molecular pathway—the PU.1–CD28 axis—that could be targeted by future immunotherapies to slow or prevent Alzheimer’s progression.
About this Alzheimer’s disease research news
Author: Maren Berghoff
Source: Max Planck Institute
Contact: Maren Berghoff – Max Planck Institute
Image: The image is credited to Neuroscience News
Original Research: Open access.
“Lymphoid gene expression supports neuroprotective microglia function” by Anne Schaefer et al. Nature
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