The paper explains that in type 2 diabetes, the same problems that make muscles waste away (sarcopenia) also hurt the brain and can lead to dementia. A key link is a group of muscle‑released signals called myokines – especially IGF‑1 – that help both muscle growth and brain health. Bad blood sugar, insulin resistance, and inflammation mess up these signals, but regular exercise and good glucose control can boost the helpful myokines and protect both muscle and mind.

Type 2 diabetes mellitus (T2DM) is increasingly recognized as a shared pathological substrate for both sarcopenia and cognitive decline, particularly Alzheimer's disease (AD). This review synthesizes current evidence on the converging molecular pathways linking insulin resistance, hyperglycaemia, mitochondrial dysfunction, oxidative stress, and chronic inflammation to muscle wasting and neurodegeneration. Central to this interplay is the muscle-brain axis, a bidirectional communication network mediated by myokines, exercise-induced cytokines that influence metabolic and neural homeostasis. Key myokines such as IGF-1, irisin, BDNF, FGF21, and SPARC promote myogenesis, synaptic plasticity, and neuroprotection, while others including myostatin, IL-8, and GDF-15 exert detrimental effects. Context-dependent molecules such as IL-6, IL-15, lactate, and cathepsin-B show dual roles modulated by aging, inflammation, and metabolic state. Emerging data support that improved glycaemic control, enhanced insulin sensitivity, and sustained physical activity can attenuate both sarcopenia and cognitive decline. This review aims to summarize current evidence describing how insulin resistance, chronic hyperglycaemia, mitochondrial dysfunction, oxidative stress, and inflammation interact to promote both muscle wasting and neurodegeneration.