A COMPREHENSIVE ANALYSIS OF TYPE 3 DIABETES: CONNECTING METABOLIC DYSFUNCTION WITH ALZHEIMER'S DISEASE

Background-Insulin resistance, which affects neural transmission and energy metabolism, is one metabolic abnormality that is increasingly linked to Alzheimer's disease (AD). Amyloid-beta buildup, tau pathology, and neuroinflammation are all exacerbated by disruption of the insulin pathways in the brain. The idea of "Type 3 Diabetes" (T3D) was born because of these common characteristics. The purpose of this study is to examine the molecular connections between AD and insulin resistance and to highlight new treatment approaches. Method- Using PubMed, Scopus, Web of Science, and the Cochrane Library, a systematic review was carried out in compliance with PRISMA standards to find publications that were published between January 2010 and July 2025. "Diabetes Mellitus," "Insulin Resistance," "Alzheimer Disease," "Nerve Degeneration," "Cognitive Dysfunction," and other relevant clinical and biological keywords were among the search terms used. The final analysis contained 213 peer-reviewed articles after duplicates were eliminated and predetermined inclusion and exclusion criteria were applied. Results- A major pathogenic factor that has been repeatedly found to affect tau phosphorylation, amyloid-beta clearance, and brain glucose uptake is insulin resistance. Insulin signaling pathway disruption, particularly PI3K/Akt and GLUT4 translocation, has been linked to oxidative stress, neuroinflammation, and cognitive impairment. Transcriptomic evidence also demonstrated how non-coding RNA’s, such as MEG3 and MALAT1, regulate insulin sensitivity and glucose homeostasis, connecting metabolic imbalance to neural dysfunction. Conclusion-The idea of T3D is supported by the fact that insulin resistance and impaired glucose metabolism are key factors in the onset and progression of AD. There is encouraging neuroprotective potential when these pathways are targeted. Validating these therapies in extensive clinical trials should be the main goal of future research.

Authors

Publication Details

Published
2025-04-11
DOI
https://doi.org/10.53555/1mp6cs91
Primary Topic
Diet and metabolism studies
Type
article
Field-Weighted Citation Impact
0.00
Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

A COMPREHENSIVE ANALYSIS OF TYPE 3 DIABETES: CONNECTING METABOLIC DYSFUNCTION WITH ALZHEIMER'S DISEASE

Komal Yadav
Diet and metabolism studies
article

A COMPREHENSIVE ANALYSIS OF TYPE 3 DIABETES: CONNECTING METABOLIC DYSFUNCTION WITH ALZHEIMER'S DISEASE

Komal Yadav
article en

Abstract

Background-Insulin resistance, which affects neural transmission and energy metabolism, is one metabolic abnormality that is increasingly linked to Alzheimer's disease (AD). Amyloid-beta buildup, tau pathology, and neuroinflammation are all exacerbated by disruption of the insulin pathways in the brain. The idea of "Type 3 Diabetes" (T3D) was born because of these common characteristics. The purpose of this study is to examine the molecular connections between AD and insulin resistance and to highlight new treatment approaches. Method- Using PubMed, Scopus, Web of Science, and the Cochrane Library, a systematic review was carried out in compliance with PRISMA standards to find publications that were published between January 2010 and July 2025. "Diabetes Mellitus," "Insulin Resistance," "Alzheimer Disease," "Nerve Degeneration," "Cognitive Dysfunction," and other relevant clinical and biological keywords were among the search terms used. The final analysis contained 213 peer-reviewed articles after duplicates were eliminated and predetermined inclusion and exclusion criteria were applied. Results- A major pathogenic factor that has been repeatedly found to affect tau phosphorylation, amyloid-beta clearance, and brain glucose uptake is insulin resistance. Insulin signaling pathway disruption, particularly PI3K/Akt and GLUT4 translocation, has been linked to oxidative stress, neuroinflammation, and cognitive impairment. Transcriptomic evidence also demonstrated how non-coding RNA’s, such as MEG3 and MALAT1, regulate insulin sensitivity and glucose homeostasis, connecting metabolic imbalance to neural dysfunction. Conclusion-The idea of T3D is supported by the fact that insulin resistance and impaired glucose metabolism are key factors in the onset and progression of AD. There is encouraging neuroprotective potential when these pathways are targeted. Validating these therapies in extensive clinical trials should be the main goal of future research.

Openalex Percentile: Top 66%
Diet and metabolism studies
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.