relationship between diabetes mellitus and Parkinson's disease. Reuven Sandyk.

[aspergerian13]

The relationship between diabetes mellitus and Parkinson's disease.

Review article.

Sandyk R.

Int J Neurosci. 1993 Mar-Apr.

ncbi.nlm.nih.gov/m/pubmed/8...

It has been reported that 50% to 80% of patients with Parkinson's disease have abnormal glucose tolerance which may be further exacerbated by levodopa therapy. Little is known about the impact of chronic hyperglycemia on the severity of the motor manifestations and the course of the disease as well as its impact on the efficacy of levodopa or other dopaminergic drugs.

This issue, which has been largely ignored, is of clinical relevance since animal studies indicate that chronic hyperglycemia decreases striatal dopaminergic transmission and increases the sensitivity of postsynaptic dopamine receptors.

In addition, evidence from experimental animal studies indicates that diabetic rats are resistant to the locomotor and behavioral effects of the dopamine agonist amphetamine. The resistance to the central effects of amphetamine is largely restored with chronic insulin therapy.

In the present communication, I propose that in Parkinson's disease diabetes may exacerbate the severity of the motor disability and attenuate the therapeutic efficacy of levodopa or other dopaminergic agents as well as increase the risk of levodopa-induced motor dyskinesias. Thus, it is advocated that Parkinsonian patients should be routinely screened for evidence of glucose intolerance and that if found aggressive treatment of the hyperglycemia may improve the response to levodopa and potentially diminish the risk of levodopa-induced motor dyskinesias.

****

A very fine review. Pmc:

Multiple Evidences for Association between Cognitive Impairment and Dysglycemia in Parkinson’s Disease: Implications for Clinical Practice.

2017.

ncbi.nlm.nih.gov/pmc/articl...

[aspergerian13]

Also:

The Relevance of Insulin Action in the Dopaminergic System.

2018.

ncbi.nlm.nih.gov/pmc/articl...

[aspergerian13 in reply to aspergerian13]

The role of endoplasmic reticulum-mitochondria contact sites in the control of glucose homeostasis: an update.

Jennifer Rieusset.

Cell Death & Disease volume 9, 388 (2018).

Open access.

nature.com/articles/s41419-...

[pvw2 in reply to aspergerian13]

Quote of link above: Conclusion

Several clinical and experimental studies indicate a higher prevalence of PD in patients diagnosed with diabetes. Indeed, it is now clear that the loss of insulin signaling may cause neuronal mitochondrial dysfunction and oxidative stress followed by loss of dopaminergic neurons and impaired memory functioning. These results have been corroborated by studies performed in animal models and by the positive action that some antidiabetic drugs induce with significant benefits in patients diagnosed with PD. However, although the scientific research has reached several promising results, further and more detailed investigations are necessary to validate these studies in order to discover new therapeutic avenues.

[pvw2]

This looks like a complex issue. For example, the the link at the end says lack of processing sugar properly in the brain causes Alzheimer's, not merely the presence of sugar as some claim. Neuropathy is common with type 2 diabetes. Excess weight and fat around the waste has been associated with increase in type 2 diabetes. Exercise is also a benefit with type 2 diabetes.

Sugar and Alzheimer’s disease: a bittersweet truth

ncbi.nlm.nih.gov/pmc/articl...

[gaga1958]

what would the aggressive treatment be?

" Thus, it is advocated that Parkinsonian patients should be routinely screened for evidence of glucose intolerance and that if found aggressive treatment of the hyperglycemia may improve the response to levodopa and potentially diminish the risk of levodopa-induced motor dyskinesias'