ASSOCIATION BETWEEN ALZHEIMER DISEASE AND DIABETES: A REVIEW OF LITERATURE


İğit T., Altındağ F., Yıldızhan K.

INTERNATIONAL ISTANBUL MODERN SCIENTIFIC RESEARCH CONGRESS–V, İstanbul, Türkiye, 9 - 11 Temmuz 2023, ss.248-250

  • Yayın Türü: Bildiri / Özet Bildiri
  • Basıldığı Şehir: İstanbul
  • Basıldığı Ülke: Türkiye
  • Sayfa Sayıları: ss.248-250
  • Van Yüzüncü Yıl Üniversitesi Adresli: Evet

Özet

ASSOCIATION BETWEEN ALZHEIMER DISEASE AND DIABETES: A REVIEW

OF LITERATURE

ABSTRACT

Alzheimer's disease is a neurodegenerative disease with a loss of cognitive function.

Cognitive problems such as neuronal damage and destruction and memory loss occur in the

early stages of the disease. Diabetes is a complex metabolic disorder characterized by

increased blood glucose levels or impaired insulin response due to altered insulin production

by pancreatic cells. It has been reported to cause structural and functional changes in the

central nervous system and abnormalities in peripheral organs in diabetic disease. For this

reason, it was assumed that there may be a relationship between diabetes and

neurodegenerative diseases. Studies have suggested that diabetes can accelerate the onset of

Alzheimer's disease and also affect cognitive functions. Although many studies on this

subject, the relationship between these two diseases is still not fully elucidated. Some

suggested mechanisms include insulin resistance, hyperglycemia, oxidative stress,

neuroinflammation, amyloid-beta deposition, and blood-brain barrier dysfunction. Among

them, it is a remarkable hypothesis that insulin resistance and hyperinsulinemia may increase

amyloid beta deposition in the brain and trigger neurodegeneration. In addition, studies have

emphasized that insulin deficiency can increase oxidative stress in cells by inhibiting glucose

uptake in neuronal cells. In addition, vascular factors, neurovascular disorders, and

inflammation are accepted as common points of both diseases. In our presentation, which we

created with a literature review, the triggering aspect of diabetes pathogenesis on Alzheimer's

disease will be mentioned, and the striking points between the common pathophysiological

mechanisms of these two diseases, which have a complex and multifactorial etiology, will be

emphasized. Given these, together with the fact that both disorders are highly heterogeneous,

the link between the two is likely to result from a combination of different molecular, cellular,

and systemic factors that are difficult to resolve. Understanding the relationship between

insulin and the brain in the pathogenesis of diabetes will help to understand the main cause of

Alzheimer's disease. In addition, further immunohistochemical studies using insulin receptor

markers in observing pathological changes in diabetic neuropathy will contribute to the

pathogenesis of Alzheimer's. We believe that further experimental and clinical studies at the

molecular level on insulin receptors and their functions in the brain may contribute to the

literature on the treatment of neurological diseases such as Alzheimer's.