This sets off a cascade of signaling molecules that result in T cells, B cells, and Macrophages to cross the blood-brain barrier and attack myelin on neuronal axons leading to inflammation. Further release of antigens drives subsequent degeneration causing increased inflammation. Multiple sclerosis presents itself as a spectrum based on the degree of inflammation, a majority of patients experience early relapsing and remitting episodes of neuronal deterioration following a period of recovery. Some of these individuals may transition to a more linear progression of the disease, while about 15% of others begin with a progressive course on the onset of Multiple sclerosis. The inflammatory response contributes to the loss of the grey matter, and as a result current literature devotes itself to combatting the auto-inflammatory aspect of the disease. While there are several proposed causal links between EBV and the HLA-DRB1*15:01 allele to the onset of MS – they may contribute to the degree of autoimmune attack and the resultant inflammation – they do not determine the onset of MS.

Amyotrophic lateral sclerosis
Amyotrophic lateral sclerosis (ALS) or Lou Gehrigs disease is a disease in which motor neurons are selectively targeted for degeneration. Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder that negatively impacts the upper motor neurons (UMNs) and lower motor neurons (LMNs). In 1993, missense mutations in the gene encoding the antioxidant enzyme Cu/Zn superoxide dismutase 1 (SOD1) were discovered in a subsets of patients with familial ALS. This discovery led researchers to focus on unlocking the mechanisms for SOD1-mediated diseases.
Osteopathia striata with cranial sclerosis (OSCS) is a rare genetic entity characterized by osseous abnormalities. Signs and symptoms
Symptoms and their severity vary person to person but generally people with OSCS have generalized dysplasia of the distal parts of the long bones, cranial sclerosis (that is, the hardening of bones in the face and head), macrocephaly (abnormally large head), and cleft palate. Developmental delay, hearing loss, congenital heart defects, alongside feeding and breathing (dyspnea) difficulties are common as well, although they are not seen in all cases. Complications
The feeding and breathing difficulties that are sometimes associated with OSCS can result in starvation, nutritional deficiencies, and/or respiratory arrest if they remain untreated, which may result in early death. Treatment
Although OSCS has no cure, it can be treated and managed. Treatment is symptom-specific, for example: avoiding areas with air pollution (e.g., big cities, smoking areas, etc. ), high-altitude areas, and physically exhausting activities can reduce breathlessness episodes (breathing difficulties). Causes
This condition is caused by X-linked dominant mutations in the AMER1 gene, in the X chromosome. Prevalence
According to OMIM, the total number of cases described in medical literature is between 70 and 90. == References ==