Paula I. Moreira

TL;DR: This review examines the neurodegenerative events associated with diabetes, highlighting the role of hyperglycemia and/or hypoglycemia on cognitive function and neuronal UCPs as possible therapeutic targets for the treatment of diabetes-associated central complications and neuro degenerative diseases, namely Alzheimer's and Parkinson's diseases.

TL;DR: Results support the idea that hydroxytamoxifen protects lipid peroxidation and inhibits the mitochondrial permeability transition pore in brain, which is pharmacologically much more potent and less toxic than its promoter tamoxifens.

TL;DR: The past and current findings that link AD and PD with T2DM, emphasizing the common pathological mechanisms are summarized and the efficacy of antidiabetic drugs in the prevention and/or treatment of AD andPD is discussed.

TL;DR: The results show that recurrent-hypoglycemia renders mitochondria more susceptible to UCPs modulation while the proton-leak of long-term hyperglycemic rats is mainly modulated by ANT, which suggest that brain cortical mitochondria have distinct adaptation mechanisms in face of different metabolic insults.

TL;DR: The results showed that skeletal muscle functionality is already affected in 3-month-old 3xTg-AD mice as evidenced by deficient acetylcholinesterase and catalase activities as well as by alterations in fatty acid composition of mitochondrial membranes, and observed significant changes in phospholipid composition of skeletal muscle tissues when compared with age-matched nonTg mice.