Current evidence suggests that obesity, in addition to being a contributing
factor for cardiovascular and metabolic disorders, also increases the risk of Alzheimer's
disease (AD). It is well-documented fact that the brain is significantly affected by the
inflammatory condition of obesity i.e. meta-inflammation via several pathways. Some
systemic inflammatory and metabolic mediators produced by adipose tissue cross the
blood-brain barrier in certain conditions. The most essential outcome is the activation
of the brain-resident microglia and astrocytes contributing to CNS inflammation.
Multiple studies have shown the existence of inflammatory markers in the brain and
serum of post-mortem AD. In addition to the role of meta-inflammation, recent
research has shown that insulin resistance and impaired insulin signaling can contribute
to the development of AD as well as other neurological disorders. With this in mind, a
group of scientists has proposed the term brain diabetes, or diabetes type 3, for
cognitive impairment in AD patients, to unify the metabolic inflammatory pathways of
the development of the disorder. The purpose of this is to show that AD is more than
just an aggregation of oligomeric and fibrillar Ab deposits in the brain tissue. The
disorder is represented by many pathological alterations, such as a lower degree of
metabolism, blood-brain-barrier disturbance, and glial activation. Although not all
signaling pathways involved in these processes are known yet, this new name could
open a new field in the treatment of neurodegenerative impairments, to either prevent
or slow down their development.
Keywords: Alzheimer disease, Antidiabetics, Diabetes type 3, Inflammasomes,
Insulin resistance, Meta-inflammation, Obesity, Proinflammatory cytokines,
TNF-α.
