- Academic Editor
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†These authors contributed equally.
The origins of late-life depression are multifaceted and remain challenging to
fully understand. While the traditional monoamine neurotransmitter hypothesis
provides some insights, it falls short in explaining the disease’s onset and
progression, leaving treatments often less than optimal. There is an emergent
need to uncover new underlying mechanisms. Among these, the “inflammation
hypothesis” has been gaining traction in scientific discussions regarding
late-life depression. There is compelling evidence linking inflammation processes
to the emergence of this form of depression. This review delves into the nuanced
relationship between inflammation and late-life depression, emphasizing the
pivotal role and implications of inflammation in its pathogenesis. Changes in
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