Neuritic plaques are abnormal protein deposits that accumulate outside nerve cells in the brain’s grey matter. While common in the aging brain, their widespread presence distinguishes certain neurodegenerative conditions.
How Neuritic Plaques Form
Neuritic plaques are primarily composed of amyloid-beta (Aβ), a protein fragment. This peptide originates from amyloid precursor protein (APP), found in cell membranes. Enzymes, specifically beta-secretase and gamma-secretase, cleave APP to produce Aβ fragments.
Once produced, amyloid-beta peptides can misfold and aggregate. They initially form small, soluble clumps called oligomers. These oligomers then combine to create insoluble fibrils, which eventually accumulate into larger, visible plaques.
Impact on Brain Health
The accumulation of neuritic plaques has consequences for brain health, particularly in conditions like Alzheimer’s disease. These deposits disrupt normal communication between neurons, impairing their function. Plaques can also lead to the degeneration of neuronal processes, known as dystrophic neurites, which are swollen or abnormal nerve endings surrounding the plaque.
Neuritic plaques can trigger an immune response within the brain, leading to neuroinflammation. Microglia and astrocytes, resident immune cells, become activated in response to amyloid-beta, releasing inflammatory molecules. This chronic inflammatory state can contribute to further neuronal damage and loss of brain tissue. Plaque burden has been linked to declines in cognitive abilities, including memory loss.
Identifying Plaques and New Approaches
Detecting neuritic plaques in living individuals has advanced with non-invasive imaging techniques. Amyloid PET (Positron Emission Tomography) scans allow for the visualization of amyloid plaque accumulation in the brain. These scans use a radioactive tracer that binds to the amyloid-beta protein, making the plaques “light up” on the scan. This enables earlier detection and monitoring.
Historically, definitive identification of neuritic plaques was only possible through post-mortem examination of brain tissue. Tissue samples from deceased individuals are stained and examined under a microscope to confirm plaque presence and density. While post-mortem analysis remains the gold standard, amyloid PET scans provide a tool for diagnosis and research in living patients.
Current research explores various strategies to address neuritic plaques. These include preventing their formation, enhancing the brain’s ability to clear existing plaques, and developing therapies to mitigate their harmful effects on neuronal function.
Plaques Versus Tangles
Neuritic plaques and neurofibrillary tangles are distinct pathological hallmarks observed in Alzheimer’s disease. Neuritic plaques are extracellular deposits, forming outside neurons. Their primary component is amyloid-beta protein.
In contrast, neurofibrillary tangles are intracellular aggregates, forming inside the neurons themselves. These tangles are composed of an abnormal form of tau protein, which becomes hyperphosphorylated and aggregates into twisted filaments. While both pathologies contribute to neurodegeneration, they do so through different mechanisms and have distinct locations within the brain.