<p>Type 2 diabetes is associated with the formation of features of Alzheimer’s disease (AD). A common mechanism appears to be the impairment of autophagy, making its stimulation a potential target for AD treatment. A good opportunity to study the correction of diabetes and neurodegeneration is provided by db/db mice, a model of diabetes and obesity that develop signs of AD with age. In our previous work, we found that db/db mice are amenable to treatment with the disaccharide trehalose, which activates autophagy via an mTOR-independent pathway. In 3-month-old mice, trehalose reduced obesity, attenuated hyperglycaemia, significantly activated autophagy in the brain, weakened neuroinflammation and oxidative stress, and restored cognitive impairment. It remains unclear to what extent the therapeutic effect of trehalose depends on the age of mice and on the activation of autophagy gene transcription and ultrastructural changes in neurons and glia cells. The therapeutic effect of treatment with 3% trehalose in drinking was investigated on 5-month-old db/db mice. Trehalose did not induce a significant decrease in the body mass or blood glucose and cholesterol levels but it decreased the expression of the insulin receptor gene <i>Insr.</i> There was a visual increase in the lipofuscin levels in cortical neurons and glial cells, while trehalose did not attenuate the accumulation of the marker. Thus, a differential effect of trehalose was obtained for 5-month-old db/db mice, consisting in the absence of activation of autophagy gene transcription or attenuation of lipofuscin accumulation. Apparently, the therapeutic effect of trehalose on the disturbances in db/db line mice decreases with age and becomes ineffective at 5 months of age.</p>