scholarly journals Alzheimer’s Disease and Empathic Abilities: The Proposed Role of the Cingulate Cortex

2021 ◽  
pp. 1-8
Author(s):  
Marina Ávila-Villanueva ◽  
Jaime Gómez-Ramírez ◽  
Jesús Ávila ◽  
Miguel A. Fernández-Blázquez
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Social Interactions ◽  
Cognitive Processes ◽  
Crucial Role ◽  
Cingulate Cortex

In recent years there has been increasing interest in examining the role of empathic abilities in Alzheimer’s disease (AD). Empathy, the ability to understand and share another person’s feelings, implies the existence of emotional and cognitive processes and is a pivotal aspect for success in social interactions. In turn, self-empathy is oriented to one’s thoughts and feelings. Decline of empathy and self-empathy can occur during the AD continuum and can be linked to different neuroanatomical pathways in which the cingulate cortex may play a crucial role. Here, we will summarize the involvement of empathic abilities through the AD continuum and further discuss the potential neurocognitive mechanisms that contribute to decline of empathy and self-empathy in AD.

scholarly journals Unawareness of deficits in Alzheimer’s disease: role of the cingulate cortex

Brain ◽  
2011 ◽  
Vol 134 (4) ◽  
pp. 1061-1076 ◽  
Author(s):  
Martina Amanzio ◽  
Diana M. E. Torta ◽  
Katiuscia Sacco ◽  
Franco Cauda ◽  
Federico D’Agata ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cingulate Cortex

scholarly journals Crucial role of calbindin-D28k in the pathogenesis of Alzheimer’s disease mouse model

2014 ◽  
Vol 21 (10) ◽  
pp. 1575-1587 ◽  
Author(s):  
S-Y Kook ◽  
H Jeong ◽  
M J Kang ◽  
R Park ◽  
H J Shin ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Crucial Role ◽  
Calbindin D28k

scholarly journals The Glucose Metabolic Pathway as A Potential Target for Therapeutics: Crucial Role of Glycosylation in Alzheimer’s Disease

2020 ◽  
Vol 21 (20) ◽  
pp. 7739
Author(s):  
Vidyasagar Naik Bukke ◽  
Rosanna Villani ◽  
Moola Archana ◽  
Agata Wawrzyniak ◽  
Krzysztof Balawender ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Metabolic Pathway ◽  
Crucial Role ◽  
Late Onset ◽  
Therapeutic Option ◽  
Three Dimensional ◽  
Post Translational Modification ◽  
Glucose Content

Glucose uptake in the brain decreases because of normal aging but this decline is accelerated in Alzheimer’s disease (AD) patients. In fact, positron emission tomography (PET) studies have shown that metabolic reductions in AD patients occur decades before the onset of symptoms, suggesting that metabolic deficits may be an upstream event in at least some late-onset cases. A decrease in availability of glucose content induces a considerable impairment/downregulation of glycosylation, which is an important post-translational modification. Glycosylation is an important and highly regulated mechanism of secondary protein processing within cells and it plays a crucial role in modulating stability of proteins, as carbohydrates are important in achieving the proper three-dimensional conformation of glycoproteins. Moreover, glycosylation acts as a metabolic sensor that links glucose metabolism to normal neuronal functioning. All the proteins involved in β-amyloid (Aβ) precursor protein metabolism have been identified as candidates of glycosylation highlighting the possibility that Aβ metabolism could be regulated by their glycosylation. Within this framework, the present review aims to summarize the current understanding on the role of glycosylation in the etiopathology of AD, emphasizing the idea that glucose metabolic pathway may represent an alternative therapeutic option for targeting AD. From this perspective, the pharmacological modulation of glycosylation levels may represent a ‘sweet approach’ to treat AD targeting new mechanisms independent of the amyloid cascade and with comparable impacts in familial and sporadic AD.

Dissecting the role of Corticotropin-releasing hormone receptor type 1 in Alzheimer's Disease

2011 ◽  
Vol 44 (06) ◽  
Author(s):  
K Lerche ◽  
M Willem ◽  
K Kleinknecht ◽  
C Romberg ◽  
U Konietzko ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Hormone Receptor ◽  
Receptor Type ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone

Role of melatonin in regulating neurogenesis: Implications for the neurodegenerative pathology and analogous therapeutics for Alzheimer’s disease

2020 ◽  
Vol 3 (2) ◽  
pp. 216-242 ◽  
Author(s):  
Mayuri Shukla ◽  
Areechun Sotthibundhu ◽  
Piyarat Govitrapong
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Adult Neurogenesis ◽  
Adult Brain ◽  
Therapeutic Approaches ◽  
Therapeutic Implications ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Progenitor Cell Proliferation

The revelation of adult brain exhibiting neurogenesis has established that the brain possesses great plasticity and that neurons could be spawned in the neurogenic zones where hippocampal adult neurogenesis attributes to learning and memory processes. With strong implications in brain functional homeostasis, aging and cognition, various aspects of adult neurogenesis reveal exuberant mechanistic associations thereby further aiding in facilitating the therapeutic approaches regarding the development of neurodegenerative processes in Alzheimer’s Disease (AD). Impaired neurogenesis has been significantly evident in AD with compromised hippocampal function and cognitive deficits. Melatonin the pineal indolamine augments neurogenesis and has been linked to AD development as its levels are compromised with disease progression. Here, in this review, we discuss and appraise the mechanisms via which melatonin regulates neurogenesis in pathophysiological conditions which would unravel the molecular basis in such conditions and its role in endogenous brain repair. Also, its components as key regulators of neural stem and progenitor cell proliferation and differentiation in the embryonic and adult brain would aid in accentuating the therapeutic implications of this indoleamine in line of prevention and treatment of AD.   

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