During recent years, numerous lines of research including proteomics and molecular biology have highlighted
multiple targets and signaling pathways involved in metabolic abnormalities and neurodegeneration. However, correlation
studies of individual neurodegenerative disorders (ND) including Alzheimer, Parkinson, Huntington and Amyotrophic
lateral sclerosis in association with Diabetes type 2 Mellitus (D2M) are demanding tasks. Here, we report a
comprehensive mechanistic overview of major contributors involved in process-based co-regulation of D2M and NDs.
D2M is linked with Alzheimer’s disease through deregulation of calcium ions thereby leading to metabolic fluctuations of
glucose and insulin. Parkinson-associated proteins disturb insulin level through ATP-sensitive potassium ion channels and
extracellular signal-regulated kinases to enhance glucose level. Similarly, proteins which perturb carbohydrate metabolism
for disturbing glucose homeostasis link Huntington, Amyotrophic lateral sclerosis and D2M. Other misleading processes
which interconnect D2M and NDs include oxidative stress, mitochondrial dysfunctions and microRNAs (miRNA29a/b
and miRNA-9). Overall, the collective listing of pathway-specific targets would help in establishing novel connections
between NDs and D2M to explore better therapeutic interventions.
Keywords: Diabetes Type 2 Mellitus, Neurodegenerative Disorders, Amyloid Precursor Protein, glucose metabolism, neuronal
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