Tauopathies are neurodegenerative brain diseases that are characterized by the formation of intraneuronal inclusions containing the microtubule-associated protein tau.
Telmisartan ameliorates inflammation in various brain disorders through angiotensin II type 1 receptor (AT1) blockade and peroxisome proliferator-activated receptor gamma (PPARγ) activation.
In this study we aimed to evaluate the pleiotropic nature of SLC6A4 alterations and their association with the overall risk of brain diseases rather than disorder-specific.
Furthermore, 10i exhibited anti-neuroinflammatory effect in vitro and in vivo via inhibiting PKM2-mediated glycolysis and NLRP3 activation, indicating PKM2 as a novel target for neuroinflammation and its related brain disorders.
Preclinical experiments and clinical trials demonstrated that angiotensin II AT<sub>1</sub> receptor overactivity associates with aging and cellular senescence and that AT<sub>1</sub> receptor blockers (ARBs) protect from age-related brain disorders.
Telmisartan ameliorates inflammation in various brain disorders through angiotensin II type 1 receptor (AT1) blockade and peroxisome proliferator-activated receptor gamma (PPARγ) activation.
Cytidine 5-diphosphocholine (CDP-choline) administration has been shown to improve learning and memory deficits in different models of brain disorders.
Orally active and blood-brain barrier-permeable specific inhibitors for cathepsin B can be potentially effective new pharmaceutical interventions against inflammatory brain diseases and brain aging.
Cytidine 5-diphosphocholine (CDP-choline) administration has been shown to improve learning and memory deficits in different models of brain disorders.
Furthermore, 10i exhibited anti-neuroinflammatory effect in vitro and in vivo via inhibiting PKM2-mediated glycolysis and NLRP3 activation, indicating PKM2 as a novel target for neuroinflammation and its related brain disorders.
Finally, with the use of transcriptomic and peptidomic techniques, dysregulations of TAARs (especially TAAR6) have been identified in brain disorders characterized by cognitive impairment.
This mechanism might contribute to cognitive impairment in chronic brain disease featuring elevated IFN-γ levels, blood-brain barrier leakage, and/or T cell infiltration, well before neurodegeneration occurs.
Our results indicate that BDNF and S100B are useful and sensitive markers of glucose metabolism disturbance and reinforce these proteins as general acute markers of brain disorders.
Despite the increasing evidence for the involvement of BDNF and neuroinflammation in brain disorders, there is scarce evidence that addresses the interaction between the neurotrophin and neuroinflammation in psychiatric and neurodegenerative diseases.
Apolipoprotein E (APOE) is implicated not only in chronic degenerative neurological diseases, such as Alzheimer's disease, but also in acute brain disorders, including traumatic brain injury.
Previous studies have indicated that the adenosine triphosphate‑sensitive homomeric P2X7 receptor (P2X7R) plays an important role and exhibits therapeutic potential in a number of brain disorders, including temporal lobe epilepsy (TLE).
S100 proteins, the largest sub-group within the EF-hand protein family, are closely associated with cardiovascular diseases, various types of cancer, inflammation and autoimmune pathologies and brain diseases.
Therefore, developing a positron emission tomography (PET) tracer for imaging of P2X7 receptors in vivo presents a promising approach to diagnose, monitor, and study neuroinflammation in a variety of brain disorders.
The membrane dopamine transporter (DAT) is involved in a number of brain disorders and its exploration by positron emission tomography (PET) imaging is highly relevant for the early and differential diagnosis, follow-up and treatment assessment of these diseases.
Our results indicate that BDNF and S100B are useful and sensitive markers of glucose metabolism disturbance and reinforce these proteins as general acute markers of brain disorders.