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Damage in the watershed region does not directly harm the areas of the brain involved in language production or comprehension; instead, the damage isolates these areas from the rest of the brain. [1] If there is damage to the frontal lobe, executive functions related to language use are often affected.
All of these lead to a difference in processing efficiency, which is often caused by damage to a cortical region in the brain (in receptive aphasia, for example, the lesion is in or near Wernicke's area); lesion location is the most important determining factor for all aphasic disorders, including paraphasia – the location of the lesion can ...
Depending on the extent of injury, the cellular response may be adaptive and where possible, homeostasis is restored. [1] Cell death occurs when the severity of the injury exceeds the cell's ability to repair itself. [2] Cell death is relative to both the length of exposure to a harmful stimulus and the severity of the damage caused. [1]
DNA damage response mechanisms trigger cell-cycle arrest, and attempt to repair DNA lesions or promote cell death/senescence if repair is not possible. Replication stress is observed in preneoplastic cells due to increased proliferation signals from oncogenic mutations.
Most damage can be repaired without triggering the damage response system, however more complex damage activates ATR and ATM, key protein kinases in the damage response system. [92] DNA damage inhibits M-CDKs which are a key component of progression into mitosis. In all eukaryotic cells, ATR and ATM are protein kinases that detect DNA damage.
Overall, they concluded that while the complexity of responses to DNA damage remains only partly understood, the idea that DNA damage accumulation with age is the primary cause of aging remains an intuitive and powerful one. [2] In humans and other mammals, DNA damage occurs frequently and DNA repair processes have evolved to compensate. [11]
It can initiate apoptosis (i.e., programmed cell death) if DNA damage proves to be irreparable. It is essential for the senescence response to short telomeres. p53 pathway: In a normal cell, p53 is inactivated by its negative regulator, mdm2. Upon DNA damage or other stresses, various pathways will lead to the dissociation of the p53 and mdm2 ...
When these breaks occur, ATM stops the cell from making new DNA (cell cycle arrest) and recruits and activates other proteins to repair the damage. Thus, ATM allows the cell to repair its DNA before the completion of cell division. If DNA damage is too severe, ATM will mediate the process of programmed cell death (apoptosis) to eliminate the ...