Alzheimer's disease (AD) is the most common form of age‐related neurodegenerative disease resulting in dementia. The current notion is that AD is based on a pathological plaque‐forming accumulation of amyloid‐β (Aβ) peptides that originate from a disturbed balance between production and removal of Aβ peptides. Loss of Aβ uptake capacity by brain microglia is linked to Aβ plaque formation and AD onset. In this issue of The EMBO Journal, Daria and colleagues show that this microglia dysfunction is reversible and that existing Aβ plaques can be cleared, suggesting that restoring microglia function may be vital for treating AD.
See also: A Daria et al
It is widely accepted that an imbalanced production versus clearance of Aβ peptides is the pathological origin of AD. Recent genome‐wide association studies have revealed various AD risk alleles that belong to innate immunity and that are functionally linked to phagocytosis (Hardy et al, 2014). Impaired uptake of Aβ peptides and microglia dysfunction was described in mouse models of AD (Hickman et al, 2008; Krabbe et al, 2013; Orre et al …
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