Fernandez Kristiansen (hockeylawyer2)

Dementia is a spectrum of neurological diseases characterized by memory impairment and cognitive decline with the pathogenesis and effective management remaining elusive. Several studies have identified a correlation between anemia and Alzheimer's disease and related dementias (ADRD); however, anemia subtypes and association with ADRD have yet to be studied conclusively. To study an association between ADRD and anemia of chronic inflammation. We conducted a retrospective case-control study of the patients, diagnosed with ADRD at Brookdale Hospital. Pair-wise comparisons between means of controls and cases in terms of iron studies and laboratory results were performed using a Mann-Whitney U test. Pair-wise comparisons between anemia subgroups (moderate and severe) were performed using a Two Sample proportion Z-Test, where for each couple of normally distributed population. There was a total of 4,517 (1,274 ADRD group; 3,243 Control group) patients. There was significant difference in hemoglobin 10.15 versus 11.04 [ -value <0.001]. Iron studies showed a significant difference in ferritin 395±488.18 versus 263±1023.4 [ < 0.001], total iron binding capacity 225±84.08 versus 266±82.30 [ < 0.001] and serum iron level 64±39.34 versus 53±41.83 [ < 0.001]. Folic acid and vitamin B12 levels were normal in both groups. Severe and moderate anemia in the ADRD group were respectively 6.2% [95% CI 4.2-8.4] and 13% [95% CI 9.8-16.2] higher. Overall, incidence of moderate-to-severe anemia was found to be 19% higher in ADRD group [95% CI 15.8-22.1]. We demonstrated an association between ADRD and anemia of chronic inflammation independent of age, renal function, and HgbA1C levels. We demonstrated an association between ADRD and anemia of chronic inflammation independent of age, renal function, and HgbA1C levels. The cause of Alzheimer's disease (AD) is poorly understood. Neurotropic microbes, particularly herpesviruses, might set off chronic neuroinflammation. Amyloid-β (Aβ) has antimicrobial properties and could represent a brain defense against infection. We searched for protein sequence alignment between herpes simplex virus type I (HSV-1) HSV-2, and Aβ. Protein data bank (pdb) structures for Aβ, HSV-1, and HSV-2 were searched on the RCSB Protein Data Bank. The protein structures were superimposed and aligned on PYMOL v 2.3.4. For HSV-1 and Aβ, amino acid residues ser549 - his569 of HSV-1 aligned closely with residues asp7 - asn27 of Aβ. For HSV-2 and Aβ, amino acid residues of HSV-2 aligned less closely than those of HSV-1 with residues of Aβ. Conjugating and binding to the same alpha helix in the HSV-1 protease, Aβ could be marking HSV-1 for attack by the immune system, providing a rapid inherited immune response to a destructive neurotropic virus that would otherwise require the more time-consuming increases and spreads. Progressive neurodegeneration and cognitive decline are the outcome.One unexplained feature of Alzheimer's disease (AD) is that the lateral entorhinal cortex undergoes neurodegeneration before other brain areas. However, this brain region does not have elevated levels of amyloid peptides in comparison with undamaged regions. What is the cause of this special vulnerability of the entorhinal cortex? One special feature of the lateral entorhinal cortex is that it projects to newborn neurons that have undergone adult neurogenesis in the dentate gyrus of the hippocampus. Neurogenesis is abnormal in human AD brains, and modulation of neurogenesis in experimental animals influences the course of AD. This complex process of neurogenesis may expose axon terminals originating from neurons of the entorhinal cortex to a unique combination of molecules that can enhance toxic effects of amyloid. Retrograde degeneration of neurons with axons terminating in the dentate gyrus provides a likely