gms | German Medical Science

Alzheimer’s disease (AD) pathology is characterized by aggregated β amyloid (Aβ) proteins, neurofibrillary tangles consisting of hyperphosphorylated tau protein and, ultimately, a loss of neurons. Autophagy (macro-autophagy) is a crucial cell survival mechanism that degrades and clears damaged organelles, invading pathogens and aggregated proteins. Dysfunctional autophagy has been associated with neurodegenerative diseases, and, more specifically, diminished autophagy in neurons is thought to contribute to the AD-specific Aβ protein aggregation. Beclin-1 (ATG 6), a key autophagic protein, recently has been shown to influence phagocytosis of Aβ in vitro in the microglia cell line BV2, and to be decreased in microglia derived from human AD patients [1]. We therefore set out to investigate the links between phagocytosis and autophagy and assessed key players of autophagy including Beclin-1 by means of western blotting and immunohistochemistry. We analyzed whole brain lysates and compared them to microglia isolated from two distinct strains of AD-like transgenic mice depositing Aβ and wild type mice of various ages. Our data provide a detailed microglia signature of autophagy proteins in response to Alzheimer-like Aβ aggregation.