Home > Journals > Panminerva Medica > Past Issues > Panminerva Medica 2020 September;62(3) > Panminerva Medica 2020 September;62(3):155-63



Publishing options
To subscribe
Submit an article
Recommend to your librarian


Publication history
Cite this article as



Panminerva Medica 2020 September;62(3):155-63

DOI: 10.23736/S0031-0808.20.03879-3


language: English

Type 3 diabetes (Alzheimer’s disease): new insight for promising therapeutic avenues

Mayuren CANDASAMY 1 , Safa A. MOHAMED ELHASSAN 2, Subrat KUMAR BHATTAMISRA 1, Wong Y. HUA 3, Lim M. SERN 3, Nurul A. BINTI BUSTHAMIN 3, Nurmaisaratulain B. MOHAMAD ILNI 3, Ng S. SHUN 3, Lim BAOHONG 3, Ng S. YA 3, Ng W. YING 3

1 Department of Life Sciences, School of Pharmacy, International Medical University, Kuala Lumpur, Malaysia; 2 School of Postgraduate Studies, International Medical University, Kuala Lumpur, Malaysia; 3 School of Pharmacy, International Medical University, Kuala Lumpur, Malaysia

Alzheimer’s disease (AD) and type 2 diabetes mellitus (T2D) are two of the most commonly occurring diseases worldwide, especially among the elderly population. In particular, the increased prevalence of AD has imposed tremendous psychological and financial burdens on society. Growing evidence suggests both AD and T2D share many similar pathological traits. AD is characterized as a metabolic disorder whereby the glucose metabolism in the brain is impaired. This closely resembles the state of insulin resistance in T2D. Insulin resistance of the brain has been heavily implicated two prominent pathological features of AD, Aβ plaques and neurofibrillary tangles. Brain insulin resistance is known to elicit a positive feed-forward loop towards the formation of AD pathology in which they affect each other in a synergistic manner. Other physiological traits shared between the two diseases include inflammation, oxidative stress and autophagic dysfunction, which are also closely associated with brain insulin resistance. In this review and depending on these underlying pathways that link these two diseases, we have discussed the potential therapeutic implications of AD. By expanding our knowledge of the overlapping pathophysiology involved, we hope to provide scientific basis to the discovery of novel therapeutic strategies to improve the clinical outcomes of AD in terms of diagnosis and treatment.

KEY WORDS: Alzheimer disease, Diabetes mellitus, type 2; Inflammation; Oxidative stress

top of page