دورية أكاديمية
أعرض في EDS

Insulin dysfunction and Tau pathology.

التفاصيل البيبلوغرافية
العنوان: Insulin dysfunction and Tau pathology.
المؤلفون: El Khoury NB; Département de Psychiatrie et Neurosciences, Faculté de Médecine, Université Laval Québec, QC, Canada ; Axe Neurosciences, Centre Hospitalier de l'Université Laval Québec, QC, Canada., Gratuze M; Département de Psychiatrie et Neurosciences, Faculté de Médecine, Université Laval Québec, QC, Canada ; Axe Neurosciences, Centre Hospitalier de l'Université Laval Québec, QC, Canada., Papon MA; Axe Neurosciences, Centre Hospitalier de l'Université Laval Québec, QC, Canada., Bretteville A; Axe Neurosciences, Centre Hospitalier de l'Université Laval Québec, QC, Canada., Planel E; Département de Psychiatrie et Neurosciences, Faculté de Médecine, Université Laval Québec, QC, Canada ; Axe Neurosciences, Centre Hospitalier de l'Université Laval Québec, QC, Canada.
المصدر: Frontiers in cellular neuroscience [Front Cell Neurosci] 2014 Feb 11; Vol. 8, pp. 22. Date of Electronic Publication: 2014 Feb 11 (Print Publication: 2014).
نوع المنشور: Journal Article; Review
اللغة: English
بيانات الدورية: Publisher: Frontiers Research Foundation Country of Publication: Switzerland NLM ID: 101477935 Publication Model: eCollection Cited Medium: Print ISSN: 1662-5102 (Print) Linking ISSN: 16625102 NLM ISO Abbreviation: Front Cell Neurosci Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: Lausanne, Switzerland : Frontiers Research Foundation, 2007-
مستخلص: The neuropathological hallmarks of Alzheimer's disease (AD) include senile plaques of β-amyloid (Aβ) peptides (a cleavage product of the Amyloid Precursor Protein, or APP) and neurofibrillary tangles (NFT) of hyperphosphorylated Tau protein assembled in paired helical filaments (PHF). NFT pathology is important since it correlates with the degree of cognitive impairment in AD. Only a small proportion of AD is due to genetic variants, whereas the large majority of cases (~99%) is late onset and sporadic in origin. The cause of sporadic AD is likely to be multifactorial, with external factors interacting with biological or genetic susceptibilities to accelerate the manifestation of the disease. Insulin dysfunction, manifested by diabetes mellitus (DM) might be such factor, as there is extensive data from epidemiological studies suggesting that DM is associated with an increased relative risk for AD. Type 1 diabetes (T1DM) and type 2 diabetes (T2DM) are known to affect multiple cognitive functions in patients. In this context, understanding the effects of diabetes on Tau pathogenesis is important since Tau pathology show a strong relationship to dementia in AD, and to memory loss in normal aging and mild cognitive impairment. Here, we reviewed preclinical studies that link insulin dysfunction to Tau protein pathogenesis, one of the major pathological hallmarks of AD. We found more than 30 studies reporting Tau phosphorylation in a mouse or rat model of insulin dysfunction. We also payed attention to potential sources of artifacts, such as hypothermia and anesthesia, that were demonstrated to results in Tau hyperphosphorylation and could major confounding experimental factors. We found that very few studies reported the temperature of the animals, and only a handful did not use anesthesia. Overall, most published studies showed that insulin dysfunction can promote Tau hyperphosphorylation and pathology, both directly and indirectly, through hypothermia.
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فهرسة مساهمة: Keywords: Alzheimer's disease; Tau phosphorylation; diabetes mellitus; kinases; phosphatases
تواريخ الأحداث: Date Created: 20140228 Date Completed: 20140325 Latest Revision: 20220311
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC3920186
DOI: 10.3389/fncel.2014.00022
PMID: 24574966
قاعدة البيانات: MEDLINE
الوصف
تدمد:1662-5102
DOI:10.3389/fncel.2014.00022