Alzheimer's disease: 120 years of research and progress

Ciurea, V; Covache-Busuioc, Razvan-Adrian; Mohan, Aurel George; Costin, Horia Petre; Voicu, Victor

doi:10.25122/jml-2022-0111

Cited by 7 publications

(6 citation statements)

References 21 publications

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“…High-mannose and complex sialylated N- glycans have been identified in paired helical filament-tau, while nicastrin contains a mixture of high-mannose, hybrid, and complex N- glycans. Phosphorylated tau has bisecting GlcNAc N- glycan structures ( Wang et al, 1996 ; Ciurea et al, 2023 ). Glycosylated tau has only been observed in the brains of patients with AD, and the reasons for this observation remain unknown ( Sato et al, 2001 ).…”

Section: Glycosylation Is Involved In the Pathogenesis And Etiology O...mentioning

confidence: 99%

“…The plasma ST6GAL1 levels in BACE1-knockout mice are only one-third of those in control mice. ST6GAL1 is markedly downregulated when co-expressed with APP, and its secretion significantly increases in BACE1-overexpressed cells, indicating that BACE1 is not only responsible for the cleavage and secretion of APP but also ST6GAL1 ( Figure 3B ); APP cleavage competes with ST6GAL1 processing ( Ciurea et al, 2023 ). Co - overexpression of BACE1 and ST6GAL1 increases the degree of soluble secretory glycoprotein rather than cell surface sialylation ( Sato et al, 2001 ).…”

Section: Sialyltransferases and Admentioning

confidence: 99%

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The alteration and role of glycoconjugates in Alzheimer’s disease

Kang,

Zhang,

et al. 2024

Front. Aging Neurosci.

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Alzheimer’s disease (AD) is a prevalent neurodegenerative disorder characterized by abnormal protein deposition. With an alarming 30 million people affected worldwide, AD poses a significant public health concern. While inhibiting key enzymes such as β-site amyloid precursor protein-cleaving enzyme 1 and γ-secretase or enhancing amyloid-β clearance, has been considered the reasonable strategy for AD treatment, their efficacy has been compromised by ineffectiveness. Furthermore, our understanding of AD pathogenesis remains incomplete. Normal aging is associated with a decline in glucose uptake in the brain, a process exacerbated in patients with AD, leading to significant impairment of a critical post-translational modification: glycosylation. Glycosylation, a finely regulated mechanism of intracellular secondary protein processing, plays a pivotal role in regulating essential functions such as synaptogenesis, neurogenesis, axon guidance, as well as learning and memory within the central nervous system. Advanced glycomic analysis has unveiled that abnormal glycosylation of key AD-related proteins closely correlates with the onset and progression of the disease. In this context, we aimed to delve into the intricate role and underlying mechanisms of glycosylation in the etiopathology and pathogenesis of AD. By highlighting the potential of targeting glycosylation as a promising and alternative therapeutic avenue for managing AD, we strive to contribute to the advancement of treatment strategies for this debilitating condition.

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Section: Glycosylation Is Involved In the Pathogenesis And Etiology O...mentioning

confidence: 99%

Section: Sialyltransferases and Admentioning

confidence: 99%

The alteration and role of glycoconjugates in Alzheimer’s disease

Kang,

Zhang,

et al. 2024

Front. Aging Neurosci.

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“…During the autopsy, Alois Alzheimer discovered the presence of neurofibrillary tangles and neuritic plaques, concluding that the disease was caused by the agglomeration of these structures. Neurofibrillary tangles—hyperphosphorylated tau proteins and neuritic plaques—aggregate beta amyloids [ 8 ]. A study conducted by Gatz et al found that environmental factors can influence to some degree the chance of developing AD in humans that have the predisposing genes [ 9 ].…”

Section: Alzheimer’s Disease (Ad)mentioning

confidence: 99%

Unraveling Molecular and Genetic Insights into Neurodegenerative Diseases: Advances in Understanding Alzheimer’s, Parkinson’s, and Huntington’s Diseases and Amyotrophic Lateral Sclerosis

Ciurea,

Mohan,

Covache-Busuioc

et al. 2023

IJMS

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Neurodegenerative diseases are, according to recent studies, one of the main causes of disability and death worldwide. Interest in molecular genetics has started to experience exponential growth thanks to numerous advancements in technology, shifts in the understanding of the disease as a phenomenon, and the change in the perspective regarding gene editing and the advantages of this action. The aim of this paper is to analyze the newest approaches in genetics and molecular sciences regarding four of the most important neurodegenerative disorders: Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis. We intend through this review to focus on the newest treatment, diagnosis, and predictions regarding this large group of diseases, in order to obtain a more accurate analysis and to identify the emerging signs that could lead to a better outcome in order to increase both the quality and the life span of the patient. Moreover, this review could provide evidence of future possible novel therapies that target the specific genes and that could be useful to be taken into consideration when the classical approaches fail to shed light.

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“…Nonetheless, the exact mechanism by which these proteins damage neurons is still unknown [88,90]. Despite AD being the leading cause of dementia worldwide and the growing population of AD patients, no new therapies have received approval for over a decade [91,92].…”

Section: Alzheimer's Disease In Briefmentioning

confidence: 99%

Mitochondrial Neurodegenerative Diseases: Three Mitochondrial Ribosomal Proteins as Intermediate Stage in the Pathway That Associates Damaged Genes with Alzheimer’s and Parkinson’s

Giudice

Pontieri

Aletta

et al. 2023

Biology

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Currently, numerous research endeavors are dedicated to unraveling the intricate nature of neurodegenerative diseases. These conditions are characterized by the gradual and progressive impairment of specific neuronal systems that exhibit anatomical or physiological connections. In particular, in the last twenty years, remarkable efforts have been made to elucidate neurodegenerative disorders such as Alzheimer's disease and Parkinson's disease. However, despite extensive research endeavors, no cure or effective treatment has been discovered thus far. With the emergence of studies shedding light on the contribution of mitochondria to the onset and advancement of mitochondrial neurodegenerative disorders, researchers are now directing their investigations toward the development of therapies. These therapies include molecules designed to protect mitochondria and neurons from the detrimental effects of aging, as well as mutant proteins. Our objective is to discuss and evaluate the recent discovery of three mitochondrial ribosomal proteins linked to Alzheimer's and Parkinson's diseases. These proteins represent an intermediate stage in the pathway connecting damaged genes to the two mitochondrial neurological pathologies. This discovery potentially could open new avenues for the production of medicinal substances with curative potential for the treatment of these diseases.

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Alzheimer's disease: 120 years of research and progress

Cited by 7 publications

References 21 publications

The alteration and role of glycoconjugates in Alzheimer’s disease

The alteration and role of glycoconjugates in Alzheimer’s disease

Unraveling Molecular and Genetic Insights into Neurodegenerative Diseases: Advances in Understanding Alzheimer’s, Parkinson’s, and Huntington’s Diseases and Amyotrophic Lateral Sclerosis

Mitochondrial Neurodegenerative Diseases: Three Mitochondrial Ribosomal Proteins as Intermediate Stage in the Pathway That Associates Damaged Genes with Alzheimer’s and Parkinson’s

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