Capgras Syndrome is a subcategory of delusional disorder. People affected by this syndrome believe that a close associate such as a friend or family member has been replaced by an identical imposter. This case report describes a 23-year-old woman with no prior psychiatric history, whom developed Capgras syndrome, via folie a deux, in the setting of poly-substance use. In this patient, a combination of Aripiprazole 10 mg daily and Escitalopram 10 mg daily were effective in resolving symptoms. Clonazepam was utilized for anxiety and Omega-3 fatty acids 1 g for anti-oxidative effects. Further studies are needed to investigate the effects of a variety of causes and treatments for Capgras Syndrome.

Attempted and completed self-enucleation, or removal of one's own eyes, is a rare but devastating form of self-mutilation behavior. It is often associated with psychiatric disorders, particularly schizophrenia, substance induced psychosis, and bipolar disorder. We report a case of a patient with a history of bipolar disorder who gouged his eyes bilaterally as an attempt to self-enucleate himself. On presentation, the patient was manic with both psychotic features of hyperreligous delusions and command auditory hallucinations of God telling him to take his eyes out. On presentation, the patient had no light perception vision in both eyes and his exam displayed severe proptosis, extensive conjunctival lacerations, and visibly avulsed extraocular muscles on the right side. An emergency computed tomography scan of the orbits revealed small and irregular globes, air within the orbits, and intraocular hemorrhage. He was taken to the operating room for surgical repair of his injuries. Attempted and completed self-enucleation is most commonly associated with schizophrenia and substance induced psychosis, but can also present in patients with bipolar disorder. Other less commonly associated disorders include obsessive-compulsive disorder, depression, mental retardation, neurosyphilis, Lesch-Nyhan syndrome, and structural brain lesions.

CDK5 is a member of the cyclin-dependent kinase family with diverse functions in both the developing and mature nervous system. The inappropriate activation of CDK5 due to the proteolytic release of the activator fragment p25 from the membrane contributes to the formation of neurofibrillary tangles and chronic neurodegeneration. At 18 months of age 3xTg-AD mice were sacrificed after 1 year (long term) or 3 weeks (short term) of CDK5 knockdown. In long-term animals CDK5 knockdown prevented insoluble Tau formation in the hippocampi and prevented spatial memory impairment. In short-term animals, CDK5 knockdown showed reduction of CDK5, reversed Tau aggregation, and improved spatial memory compared to scrambled treated old 3xTg-AD mice. Neither long-term nor short-term CDK5 knock-down had an effect on old littermates. These findings further validate CDK5 as a target for Alzheimer's disease both as a preventive measure and after the onset of symptoms.

β-site APP cleaving enzyme 1 (BACE1) initiates APP cleavage, which has been reported to be an inducer of tau pathology by altering proteasome functions in Alzheimer's disease (AD). However, the exact relationship between BACE1 and PHF (Paired Helical Filaments) formation is not clear. In this study, we confirm that BACE1 and Hsc70 are upregulated in the brains of AD patients, and we demonstrate that both proteins show enhanced expression in lipid rafts from AD-affected triple transgenic mouse brains. BACE1 targeting increased Hsc70 levels in the membrane and cytoplasm fractions and downregulated Hsp90 and CHIP in the nucleus in the hippocampi of 3xTg-AD mice. However, these observations occurred in a proteasome-independent manner in vitro. The BACE1miR-induced reduction of soluble hyperphosphorylated tau was associated with a decrease in MAPK activity. However, the BACE1 RNAi-mediated reduction of hyperphosphorylated tau was only blocked by 3-MA (3-methyladenine) in vitro, and it resulted in the increase of Hsc70 and LAMP2 in lipid rafts from hippocampi of 3xTg-AD mice, and upregulation of survival and homeostasis signaling. In summary, our findings suggest that BACE1 silencing neuroprotects reducing soluble hyperphosphorylated tau, modulating certain autophagy-related proteins in aged 3xTg-AD mice.