CELL: Tau protein acetylation connects traumatic brain injury and Alzheimer's disease

Traumatic brain injury (TBI) is usually caused by car accidents, falls, contact sports, or assaults.

At present, the treatment of TBI is mainly focused on stabilizing the patient's condition and relieving symptoms.

In fact, a recent small autopsy study reported an increase in the acetylation of tau at lysine (K) 280 in the brains of 3 AD patients and 3 patients with chronic traumatic encephalopathy.

However, these studies did not establish the driving force or pathological significance of the findings.

Recently, researchers published a report in Cell that TBI can induce tau acetylation (ac-tau) , which is also present in human brains with AD.

S-nitrosylation of GAPDH mediates an increase in tau acetylation

Blocking the S-nitrosylation of GAPDH, inhibiting p300/CBP, or activating Sirtuin1 can all reduce neurodegeneration, neurobehavioral disorders and the accumulation of acetylated tau in the blood and brain of mice after TBI.

In AD patients with a history of TBI, the increase of acetylated tau protein in the brain will be further enhanced , and patients receiving p300/CBP inhibitor salsalate or diflunisal showed adecrease in the incidence ofAD and clinically diagnosed TBI.

Original source:

Min-Kyoo Shin et al.