Classification and Pathophysiology of Alzheimer's Disease

Classification

• Alzheimer's with dementia.

Until now there are differing opinions about the relationship between Alzheimer's and vascular dementia.

Some scientists believe that vascular dementia is on track aterogenis dyslipidemia, especially with a short chain and unsaturated LDL, carotid atherosclerosis, high systolic blood pressure and an increase in the ratio of IR-UII (English: plasma levels of immunoreactive), while Alzheimer's is on another track, namely hiposomatomedinemia and hypogonadism.

Another scientist found as pathogens of vascular dementia that accompanies Alzheimer's on track inflammation of atherosclerosis, or even suggested that atherosclerosis is an inflammatory trigger hypoperfusion of the brain and result in Alzheimer's.

• Alzheimer accompanied by ataxia.

• or a combination of both.

Pathophysiology

Simtoma Alzheimer's is characterized by changes that are degenerative in some neurotransmitter systems, including changes in the function of neural systems that release monoaminergik glutamic acid, noradrenaline, serotonin and a series of systems that are controlled by neurotransmitters. Degenerative changes also occurred in several areas of the brain such as the temporal lobe and parietal lobe, and parts of the frontal cortex and cingulate gyrus, followed by the loss of nerve cells and synapses.

Sekretase- and presenilin-1 is an enzyme that functions to slice the C-terminus domain in AAP and release molecules from the kinesin enzyme cluster. Apoptosis occurs in nerve cells covered the amyloid plaques that still contained the C-terminus of the molecule, and does not occur if the molecule has been cut. This is inferred by the team of Howard Hughes Medical Institute, led by Lawrence S. B. Goldstein, the terminus-C carrying the signal to the neuron apoptosis. Signal apoptosis was also expressed by proNGF is not cut, when bound to p75NTR neurotrofin perceiving, and sortilin hormone stimulated.

Suspected due to the buildup of plaque induced apolipoprotein-E, which acts as kaperon protein, vitamin B1 defiensi controlling cerebral glucose metabolism such as O-GlkNAsilasi, and the lack of an enzyme that is made up of complex compounds such as thiamine-alpha ketoglutarate dehydrogenase complex, pyruvate dehydrogenase, transketolase, O- GlcNAc transferase, protein phosphatase 2A, and beta-N-asetilglukosaminidase. This resulted in an increase in cerebrospinal zalir pressure, decreasing the ratio of the hormone CRH, and igniting simtoma hypoglycemia in the brain, although the body has hyperglycemia.

In addition to presenilin-1 enzyme dysfunction that triggers simtoma ataxia, there are enzymes that cause Cdk5 and GSK3beta hiperfosforilasi tau protein, to form a pile PHF. Hiperfosforilasi also be a barrier formed between protein ligation S100beta and tau, and cause neurita dystrophy, although the zinc metabolic disorders may also prevent ligation.

Simtoma induces hyperinsulinemia and hyperglycemia also hiperfosforilasi protein tau and amyloid-beta oligomerasi which resulted in the accumulation of amyloid plaques. But despite oligomerasi induces insulin amyloid-beta, insulin also inhibits the enzyme activity of the enzyme and kaspase kaspase-9-3 that also carry signals apoptosis, and stimulates the secretion of Hsp70 by LAN5 cell to cell activating defense programs.

There is a minor controversy with allegations that hiperfosforilasi was caused by a latent infection by measles virus, or Borrelia. Seven of the 10 cases examined by the Alzheimer's McLean Hospital Brain Bank of Harvard University, suggests this kind of infection.