Cited by 51Stress Responses and CortisolParkinson's Disease Mechanisms and TreatmentsDementia and Cognitive Impairment Research

Diabetes type II: A risk factor for depression-Parkinson–Alzheimer?

Riederer, Peter, Bartl, Jasmin, Laux, Gerd, Grünblatt, Edna·2011·Neurotoxicity Research

Abstract

There is ample evidence that impairments in the hypothalamic-pituitary-adrenal (HPA) axis are of etiopathobiochemical importance in a subgroup of patients with "depression", causing hypercortisolaemia as major metabolic effect. Chronic hypercortisolaemia causes insulin resistance. Therefore, it is not surprising that epidemiological studies demonstrate an association of "depression" with diabetes type II and vice versa. Chronic stress and hypercortisolaemia are conditions, which have been suggested to be causal for Alzheimer's disease (AD) as brain insulin resistance is associated with β-Amyloid-accumulation and hyperphosphorylation of tau-protein. Depression is one of the significant symptomatology preceding AD. It is however, not known whether "depression" associated with hypercortisolaemia is the subgroup at risk for AD. In contrast to a subgroup of "depression" and to AD, in Parkinson's disease (PD) there is only weak evidence for an association with diabetes type II and insulin resistance. As "depression" is preceding PD in up to half of such patients, it remains to be elucidated whether this is a subgroup of depressed patients, which is not associated with disturbances of the HPA axis and hypercortisolaemia. Improved clinical and biochemical/molecular knowledge about "depression" associated with AD and PD in comparison to "pure" depression might lead to improved therapeutic strategies and even drug development focusing subtypes of "depression".

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Crossref · 10.1007/s12640-010-9203-1

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  • Clinical studies have revealed that type 2 diabetes patients are at higher risk of developing AD.

    “In a recent and surprising twist in the Alzheimer field, clinical studies have revealed that type 2 diabetes patients are at higher risk of developing AD (for reviews, see (Carlsson, 2010; Kopf and Frolich, 2009; Riederer et al., 2011)).”

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Authors
Riederer, P., Bartl, J., Laux, G., & Grünblatt, E.
Affiliations
  • University of Würzburg (DE)
  • Inn-Salzach-Klinikum (DE)
  • University of Zurich (CH)
Corresponding author
Grünblatt, Edna
Venue
Neurotoxicity Research
Published
2010-06-15
Volume
19
Issue
2
Pages
253-265
ISSN
  • 1029-8428 (ISSN-L)
  • 1476-3524
OpenAlex
W2007849320
Cited by
51
References
179
Citations by year
2025: 1 · 2024: 4 · 2023: 3 · 2022: 4 · 2021: 3 · 2020: 2 · 2018: 2 · 2017: 2 · 2016: 3 · 2015: 4 · 2014: 4 · 2013: 4 · 2012: 10
FWCI
0.53
Type
journal article
Language
en
Open access
closed
Locations
  • Neurotoxicity Research (publishedVersion)
  • PubMed (publishedVersion)
  • Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
type 2 diabetes, depression, Parkinson's disease, Alzheimer's disease, hypothalamic-pituitary-adrenal axis, hypercortisolism, insulin resistance, chronic stress, brain insulin resistance, amyloid accumulation, tau hyperphosphorylation, depression subtypes
MeSH terms
Alzheimer Disease, Animals, Depression, Diabetes Mellitus, Type 2, Humans, Hypothalamo-Hypophyseal System, Insulin Resistance, Parkinson Disease, Pituitary-Adrenal System, Risk Factors

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