In Alzheimers disease, tau undergoes chemical changes, becoming hyperphosphorylated; it then begins to pair with other threads, creating neurofibrillary tangles and disintegrating the neurons transport system. Pathogenic tau can also cause neuronal death through transposable element dysregulation. Disease mechanism
Exactly how disturbances of production and aggregation of the beta-amyloid peptide give rise to the pathology of Alzheimers disease is not known. The amyloid hypothesis traditionally points to the accumulation of beta-amyloid peptides as the central event triggering neuron degeneration. Accumulation of aggregated amyloid fibrils, which are believed to be the toxic form of the protein responsible for disrupting the cells calcium ion homeostasis, induces programmed cell death (apoptosis). It is also known that Aβ selectively builds up in the mitochondria in the cells of Alzheimers-affected brains, and it also inhibits certain enzyme functions and the utilisation of glucose by neurons.Various inflammatory processes and cytokines may also have a role in the pathology of Alzheimers disease. Inflammation is a general marker of tissue damage in any disease, and may be either secondary to tissue damage in Alzheimers disease or a marker of an immunological response. There is increasing evidence of a strong interaction between the neurons and the immunological mechanisms in the brain. Obesity and systemic inflammation may interfere with immunological processes which promote disease progression.Alterations in the distribution of different neurotrophic factors and in the expression of their receptors such as the brain-derived neurotrophic factor (BDNF) have been described in Alzheimers disease.
In humans, Erysipelothrix rhusiopathiae infections most commonly present in a mild cutaneous form known as erysipeloid  or fish poisoning. E. rhusiopathiae can cause an indolent cellulitis, more commonly in individuals who handle fish and raw meat. Erysipelothrix rhusiopathiae also causes Swine Erysipelas. It is common in domestic pigs and can be transmitted to humans who work with swine. It gains entry typically by abrasions in the hand. Bacteremia and endocarditis are uncommon but serious sequelae. Due to the rarity of reported human cases, E. rhusiopathiae infections are frequently misidentified at presentation. Diagnosis
Violaceous swelling with severe pain but without pus (Which differentiates from pus forming streptococcal and staphylococcal erysipelas)

Erysipeloid of Rosenbach
Erysipeloid of Rosenbach is a cutaneous condition most frequently characterized by a purplish marginated swelling on the hands. : 264  The eponym Rosenbachs disease is in reference to the milder type of the condition and is named after Friedrich Julius Rosenbach. Early work on the condition in US fishermen was carried out by Klaunders and colleagues. Treatment
The treatment of choice is a single dose of benzathine benzylpenicillin given by intramuscular injection, or a five-day to one-week course of either oral penicillin or intramuscular procaine benzylpenicillin. Erythromycin or doxycycline may be given instead to people who are allergic to penicillin. E. rhusiopathiae is intrinsically resistant to vancomycin. See also
Erysipeloid of Rosenbach

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