Immune dysfunction and inflammation have been found to play significant roles in Alzheimer’s disease. An analysis of brain tissue in an animal model reveals a potential for immune system dysfunction at the onset of AD. A new study reported in MedicalXpress, and first published in the journal Alzheimer’s Disease on April 15, 2025, suggests that there is a link between the progression of AD and inborn immune memory, neuroinflammation, and cellular plasticity, which is a cell’s ability to alter its function according to external stimuli while not altering underlying DNA.

Past history involving tau and amyloid proteins is now considered to be “established science”. There is also increasing evidence that implicates glia cells (brain tissue), which are part of the central nervous system and possibly another contributing cause of the disorder.

The AD study builds on current data such as evaluating whether trained immunity is a contributor to the disease cascade. Importantly, the “cascade” is a series of medical events occasionally caused by misdiagnosis, by a mistake or even by a medical error.

Innate vs. Adaptive Immune Cells

The body’s immediate line of defense against foreign invaders is innate immune cells. There are also adaptive immune cells employ a more targeted response. These cells rely on memory which, after the initial exposure, allows them to mount stronger responses in the future.

Dr. Domenico Praticò, Founding Director at Temple University’s Alzheimer’s Center, stated that their findings highlight the roles of inflammation enhancement and trained immunity that initiate a cycle of malfunctioning immune responses. This includes neuroinflammation and cellular reprogramming each contributing to the progression of AD. 

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