Neurogenesis in the Central Nervous System: Cell Cycle Progression/Exit and Differentiation of Neuronal Progenitors

Author(s):  
Dimitra Thomaidou ◽  
Panagiotis K. Politis ◽  
Rebecca Matsas
2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Yang Tian ◽  
Chen Fu ◽  
Yifan Wu ◽  
Yao Lu ◽  
Xuemei Liu ◽  
...  

Exosomes are a type of extracellular vesicles secreted by almost all kinds of mammalian cells that shuttle “cargo” from one cell to another, indicative of its role in cell-to-cell transportation. Interestingly, exosomes are known to undergo alterations or serve as a pathway in multiple diseases, including neurodegenerative diseases. In the central nervous system (CNS), exosomes originating from neurons or glia cells contribute to or inhibit the progression of CNS-related diseases in special ways. In lieu of this, the current study investigated the effect of CNS cell-derived exosomes on different neurodegenerative diseases.


2011 ◽  
Vol 193 (2) ◽  
pp. 397-407 ◽  
Author(s):  
Céline Caillava ◽  
Renaud Vandenbosch ◽  
Beata Jablonska ◽  
Cyrille Deboux ◽  
Giulia Spigoni ◽  
...  

The specific functions of intrinsic regulators of oligodendrocyte progenitor cell (OPC) division are poorly understood. Type 2 cyclin-dependent kinase (Cdk2) controls cell cycle progression of OPCs, but whether it acts during myelination and repair of demyelinating lesions remains unexplored. Here, we took advantage of a viable Cdk2−/− mutant mouse to investigate the function of this cell cycle regulator in OPC proliferation and differentiation in normal and pathological conditions. During central nervous system (CNS) development, Cdk2 loss does not affect OPC cell cycle, oligodendrocyte cell numbers, or myelination. However, in response to CNS demyelination, it clearly alters adult OPC renewal, cell cycle exit, and differentiation. Importantly, Cdk2 loss accelerates CNS remyelination of demyelinated axons. Thus, Cdk2 is dispensable for myelination but is important for adult OPC renewal, and could be one of the underlying mechanisms that drive adult progenitors to differentiate and thus regenerate myelin.


2004 ◽  
Vol 77 (1) ◽  
pp. 35-53 ◽  
Author(s):  
Milena Penkowa ◽  
Albert Quintana ◽  
Javier Carrasco ◽  
Mercedes Giralt ◽  
Amalia Molinero ◽  
...  

Author(s):  
Timothy M. O’Shea ◽  
Alexander L. Wollenberg ◽  
Alexander M. Bernstein ◽  
Darren B. Sarte ◽  
Timothy J. Deming ◽  
...  

1986 ◽  
Vol 6 (10) ◽  
pp. 2829-2836 ◽  
Author(s):  
D Schubert ◽  
B Brass ◽  
JP Dumas

2019 ◽  
Vol 20 (4) ◽  
pp. 974 ◽  
Author(s):  
Valeria Gasperi ◽  
Matteo Sibilano ◽  
Isabella Savini ◽  
Maria Catani

Niacin (also known as “vitamin B3” or “vitamin PP”) includes two vitamers (nicotinic acid and nicotinamide) giving rise to the coenzymatic forms nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP). The two coenzymes are required for oxidative reactions crucial for energy production, but they are also substrates for enzymes involved in non-redox signaling pathways, thus regulating biological functions, including gene expression, cell cycle progression, DNA repair and cell death. In the central nervous system, vitamin B3 has long been recognized as a key mediator of neuronal development and survival. Here, we will overview available literature data on the neuroprotective role of niacin and its derivatives, especially focusing especially on its involvement in neurodegenerative diseases (Alzheimer’s, Parkinson’s, and Huntington’s diseases), as well as in other neuropathological conditions (ischemic and traumatic injuries, headache and psychiatric disorders).


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