The role of tau-protein in the diagnosis of cognitive impairment in diabetes

Author(s):  
Mariia Matveeva ◽  
Julia Samoilova ◽  
Natalie Zhukova
2018 ◽  
Vol 12 (1) ◽  
pp. 50-56 ◽  
Author(s):  
Ricardo B. Maccioni ◽  
Andrea González ◽  
Víctor Andrade ◽  
Nicole Cortés ◽  
José Pablo Tapia ◽  
...  

Background:Alzheimer’s Disease (AD) is a severe neurodegenerative disorder that includes the occurrence of behavioral disorders as well as memory and cognitive impairment as major symptoms. AD affects around 12% of the aged population in the world. Considerable research efforts have pointed to the role of innate immunity as the main culprit in the pathogenesis of AD. In this context, and according to with our neuroimmunomodulation theory, microglial activation modifies the cross-talks between microglia and neurons. We postulated that glial activation triggered by “damage signals” activates a pathological molecular cascade that finally leads to hyperphosphorylation and oligomerization of the tau protein. Interestingly, these modifications correlate with the gradual cognitive impairment of patients with the AD. Microglial activation is determined by the nature and strength of the stimulus. In the AD, a continuous activation state of microglia appears to generate neuronal injury and neurodegeneration, producing the outflow of pathological tau from the inner of neurons to the extraneuronal space. Released tau, together with the contribution of ApoE4 protein, would then produce reactivation of microglia, thus inducing a positive feedback that stimulates the vicious cycle in neurodegeneration.Conclusion:Nevertheless, from the pathophysiological perspective AD is significantly more than a loss of memory. In the initial stages of AD pathogenesis, variations in the dopaminergic pathway along with serotonin diminution play an important role. This may explain why depression is associated with the onset of AD. All these pathophysiological events take place together with immunomodulatory changes that trigger tau oligomerization in the course of neurofibrillary tangles formation. Interestingly, mood disorders appear to be followed by neuroinflammatory processes and structural/functional alterations that lead to cognitive impairment in the context of AD.


2020 ◽  
Vol 4 (9) ◽  
pp. 578-583
Author(s):  
E.V. Mityaeva ◽  
◽  
P.R. Kamchatnov ◽  

Atrial fibrillation (AF) is an important medical and social problem due to its wide prevalence in the population and high risk of embolic complications leading to severe consequences. The article describes an association established between AF and an increased risk of cognitive impairment (CI). Cardioembolic stroke due to AF is a common cause of CI, however, there are other mechanisms for CI development. The article also examines the role of small vessel disease and asymptomatic cerebral infarction in the formation of CI in patients with AF. Adding that, it provides data on the AF role in the development of neurodegenerative process with the accumulation of amyloid and tau protein in the brain tissue. There is an increased risk of Alzheimer’s disease in patients with AF, although the causal relationship of these conditions requires clarification. Modern data concerning the role of neuroinflammation and genetic predisposition in the development of CI in AF were analyzed. The conclusion is made about the pathogenetic heterogeneity of higher cerebral functions disorders on the basis of the presented data on the CI pathogenetic mechanism in patients with AF and comorbid conditions. It was suggested that the optimal pathogenetic therapy can be chosen taking into account the known CI pathogenetic mechanisms. KEYWORDS: atrial fibrillation, cognitive impairment, dementia, Alzheimer’s disease, cardioembolic stroke, small vessel disease, neurodegeneration, amyloid, tau protein, pathogenesis. FOR CITATION: Mityaeva E.V., Kamchatnov P.R. Cognitive impairment in patients with atrial fibrillation. Russian Medical Inquiry. 2020;4(9):578–583. DOI: 10.32364/2587-6821-2020-4-9-578-583.


2018 ◽  
Vol 17 (5) ◽  
pp. 325-337 ◽  
Author(s):  
Hojjat Borna ◽  
Kasim Assadoulahei ◽  
Gholamhossein Riazi ◽  
Asghar Beigi Harchegani ◽  
Alireza Shahriary

Background & Objective: Neurodegenrative diseases are among the most widespread lifethreatening disorders around the world in elderly ages. The common feature of a group of neurodegenerative disorders, called tauopathies, is an accumulation of microtubule associated protein tau inside the neurons. The exact mechanism underlying tauopathies is not well-understood but several factors such as traumatic brain injuries and genetics are considered as potential risk factors. Although tau protein is well-known for its key role in stabilizing and organization of axonal microtubule network, it bears a broad range of functions including DNA protection and participation in signaling pathways. Moreover, the flexible unfolded structure of tau facilitates modification of tau by a wide range of intracellular enzymes which in turn broadens tau function and interaction spectrum. The distinctive properties of tau protein concomitant with the crucial role of tau interaction partners in the progression of neurodegeneration suggest tau and its binding partners as potential drug targets for the treatment of neurodegenerative diseases. Conclusion: This review aims to give a detailed description of structure, functions and interactions of tau protein in order to provide insight into potential therapeutic targets for treatment of tauopathies.


2020 ◽  
Vol 9 (1) ◽  
pp. 1-9
Author(s):  
Michelle C. Johansen ◽  
Nicole Langton-Frost ◽  
Rebecca F. Gottesman

2021 ◽  
Vol 22 (15) ◽  
pp. 7887
Author(s):  
Carmen Nanclares ◽  
Andres Mateo Baraibar ◽  
Alfonso Araque ◽  
Paulo Kofuji

Recent studies implicate astrocytes in Alzheimer’s disease (AD); however, their role in pathogenesis is poorly understood. Astrocytes have well-established functions in supportive functions such as extracellular ionic homeostasis, structural support, and neurovascular coupling. However, emerging research on astrocytic function in the healthy brain also indicates their role in regulating synaptic plasticity and neuronal excitability via the release of neuroactive substances named gliotransmitters. Here, we review how this “active” role of astrocytes at synapses could contribute to synaptic and neuronal network dysfunction and cognitive impairment in AD.


Nutrients ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 2118
Author(s):  
Alina Mihaela Dimache ◽  
Delia Lidia Șalaru ◽  
Radu Sascău ◽  
Cristian Stătescu

The burden of cognitive disorders is huge and still growing, however the etiology and the degree of cognitive impairment vary considerably. Neurodegenerative and vascular mechanisms were most frequently assessed in patients with dementia. Recent studies have shown the possible involvement of triglycerides levels in cognitive function through putative mechanisms such as brain blood barrier dysfunction or amyloid metabolism imbalance, but not all research in the field found this association. Several clinical studies evaluated the relationship between different forms of cognitive decline and levels of serum triglycerides, independent of other cardiovascular risk factors. This review focuses on the role of triglycerides in cognitive decline, cerebral amyloidosis and vascular impairment. Considering that the management of hypertriglyceridemia benefits from lifestyle modification, diet, and specific drug therapy, future studies are requested to appraise the triglycerides–cognitive impairment relationship.


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