Understanding the underlying biology of Alzheimer’s disease
Alzheimer’s disease is a complex brain disorder that gradually destroys memory and thinking skills. At its core, the biology of Alzheimer’s involves changes in the brain that disrupt how nerve cells communicate and survive.
One key feature is the buildup of abnormal protein fragments called amyloid-beta (Aβ). These fragments come from a larger protein known as amyloid precursor protein (APP). Enzymes called β-secretase and γ-secretase cut APP into smaller pieces, including Aβ peptides. When these peptides accumulate excessively, they clump together to form sticky plaques between nerve cells. These plaques are thought to trigger harmful processes in the brain, damaging neurons and leading to memory loss.
The enzyme γ-secretase plays an especially important role because it controls the final step in producing Aβ peptides. Changes in how γ-secretase works can increase Aβ production, worsening plaque buildup. Scientists are exploring ways to target this enzyme to reduce harmful peptide formation and protect brain cells.
Besides amyloid plaques, another hallmark of Alzheimer’s is neurofibrillary tangles—twisted fibers inside neurons made from a protein called tau. These tangles interfere with nutrient transport within nerve cells, causing them to malfunction and die over time.
Recent research also highlights inflammation as a significant factor in Alzheimer’s progression. Immune cells like neutrophils become more active around certain types of amyloid plaques, releasing enzymes such as myeloperoxidase (MPO) that may contribute to tissue damage. This suggests that immune responses might worsen neuron injury alongside plaque accumulation.
All these biological changes—amyloid plaque buildup, tau tangles inside neurons, and chronic inflammation—combine over years or decades to impair brain function progressively. The exact triggers for these processes remain unclear but likely involve genetic factors along with aging-related changes.
Understanding these underlying mechanisms helps researchers develop new treatments aimed at slowing or stopping disease progression by targeting specific steps like reducing toxic proteins or calming harmful immune activity within the brain. This ongoing work brings hope for better therapies against Alzheimer’s disease in the future.
