Mice receiving endothelium-derived amyloid and tau proteins <i>via</i> intracerebroventricular injection exhibit a learning and memory deficit in object recognition, fear conditioning, and Morris water maze studies.
The data observed show that neonatal immune activation may be associated with visuospatial memory impairment, neuroinflammation, and increased expression of GSK-3<i>β</i> and Tau proteins in the long term.
Study of molecular mechanisms of learning and memory impairment in neonatal rats post intrauterine distress via the pathway of Tau protein hyperphosphorylation.
However, the exact mechanism through which arctigenin improves amyloid beta-induced memory impairment by inhibiting the production of the hyperphosphorylated tau protein is unknown.
The associations between the loops and behaviours further suggest that tau protein pathway genes do play a significant role in non-episodic memory impairment.
We show for the first time that hippocampal GABAergic function is impaired by pathological tau protein, leading to altered synaptic plasticity and severe memory deficits.
At clinical presentation, familial FTLD-TDP patients were older at onset (p = 0.030) and had more memory deficits (p = 0.011), whereas patients with MAPT had more naming deficits (p < 0.001) and obsessive-compulsive behavior (p = 0.001).
Alzheimer's disease (AD) is defined by senile plaques made of amyloid-beta peptide (Abeta), neurofibrillary tangles made of hyperphosphorylated tau proteins, and memory deficits.