Immune mechanisms in the progression and treatment of Alzheimer`s disease

Alzheimer’s disease (AD) is the most common form of dementia, with prevalence progressively increasing with aging. Pathological hallmarks of the disease include accumulation of amyloid-beta (Aβ) peptides and neurofibrillary tangles in the brain associated with glial activation, synpatotoxicity and neural loss. In addition, AD involves age-related lymphocyte dysfunctioning, declined immunity, chronic inflammation, glial senescence and impaired brain-immune interactions. The lecture demonstrates cellular and molecular inflammatory changes in the brain caused following the accumulation and deposition of Ab. I will then show novel aspects of brain-immune interactions essential to maintain a proper glial response to Aβ. As CD4 T lymphocytes are critical in the orchestration of immunity and tissue repair throughout life, I will demonstrate changes in the CD4 T-cell landscape with aging which may lead to dysregulated inflammation and a declined tissue repair capacity that facilitate neurotoxicity and cognitive decline. Finally, I will discuss immunotherapeutic approaches for AD aimed to repairing the dialogue between the immune system and the brain.