Naslov
ACCUMULATION OF PHOSPHORYLATED TAU CONTRIBUTES TO CORTICAL PATHOLOGY FOLLOWING TRAUMATIC BRAIN INJURY IN MICE

Autori
Janković, Tamara ; Dolenec, Petra ; Pilipović, Kristina

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
MIND & BRAIN 61st INTERNATIONAL NEUROPSYCHIATRIC CONGRESS / - , 2022, 48-48

Skup
MIND & BRAIN - 61st International Neuropsychiatric Congress

Mjesto i datum
Online;, 26.05.2022. - 29.05.2022

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
Amyloid-beta precursor protein, TAU protein, Cortex, Traumatic brain injury

Sažetak
Introduction/Objectives: Traumatic brain injury (TBI) is the leading cause of death and disability that significantly burdens the health care system and society. Primary brain injury is irreversible, while secondary TBI includes pathophysiological processes that evolve over time and lead to memory and cognitive impairment. Along with the genetic predisposition, TBI is considered a risk factor for the development of Alzheimer's disease (AD). This study aimed to investigate changes in the expression of amyloid-beta precursor protein (APP) and Tau, two major proteins involved in the AD pathogenesis, in the brain cortex of C57BL/6 mice at 14 days following single moderate TBI. Participants, Materials/Methods: Lateral fluid percussion injury was used to induce a single moderate TBI over the left parietal cortex. Animals were sacrificed 14 days after injury and their cortices were prepared for Western blot or immunohistological analyses. Mice subjected to sham injury were used as a control group and were sacrificed 1 day after the sham procedure. Results: Loss of cortical NeuN positive neurons was evident in the area of the greatest brain damage but also in the pericontusional area. Subacute cortical changes in the APP expression were not detected, but cells positive to phosphorylated Tau protein were observed in the damaged cortex of brain-injured mice. Conclusions: Our preliminary results showed that single brain trauma causes loss of cortical neurons and Tau phosphorylation, without evident APP changes at 14 days post-injury. This work was supported by the University of Rijeka, Croatia, project number uniri-biomed-18-199 to K.P.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti, Biotehnologija u biomedicini (prirodno područje, biomedicina i zdravstvo, biotehničko područje)

POVEZANOST RADA