TY  - JOUR
AU  - Mago, Helen Cyntia
AU  - Besin, Valentinus
AU  - Prodjohardjono, Astuti
AU  - Vidyanti, Amelia Nur
AU  - Ervina, Waode Fifin
AU  - Humardani, Farizky Martriano
AU  - Mulyanata, Lisa Thalia
PY  - 2026
DA  - 2026/08/21
TI  - The Role of Adaptive Immune Response in Alzheimer’s Disease: Focus on Amyloid Beta-Reactive T Cells and Amyloid Beta-Specific Antibodies
JO  - OBM Neurobiology
SP  - 346
VL  - 10
IS  - 03
AB  - Alzheimer’s disease is one of the most prevalent neurodegenerative diseases among older people. Generally, there are two main pathologies of Alzheimer’s disease, including the accumulation of amyloid beta and the hyperphosphorylation of the microtubule-associated Tau protein in the brain. Recently, more studies have discovered that changes in the immune system can be one of the causes of amyloid-beta deposits. Amyloid-beta is a product of the breakdown of the glycoprotein amyloid precursor protein, a transmembrane protein that is cleaved by β-secretase and γ-secretase. In the brain, amyloid-beta deposits can trigger microglia activation, which helps eliminate the deposits. However, microglia activation may induce neuroinflammation by releasing pro-inflammatory cytokines and damage the blood-brain barrier, which can cause an influx of peripheral immune cells, including the adaptive immune system, into the brain. The role of the adaptive immune system in Alzheimer’s disease pathology is quite complicated and may alter due to aging. Aging can directly alter the immune system by reducing protective immunity through reduced production of naïve T cells and increased memory T cells. The increase in memory T cells, which have already recognized specific antigens, such as amyloid beta, may act as amyloid beta-reactive T cells and induce activation and release of amyloid beta-specific antibodies from B cells. This condition increases neuroinflammatory processes. Several drugs that directly target the immune system showed promising results as Alzheimer’s disease progressed. However, due to limited data, inconsistent results, and late adverse outcome effects, these drugs still require further research.
SN  - 2573-4407
UR  - https://doi.org/10.21926/obm.neurobiol.2603346
DO  - 10.21926/obm.neurobiol.2603346
ID  - Mago2026
ER  -