Alzheimer Cause

The reason, in particular, Alzheimer's disease is known for the moment (except in the cases of genetic differences found in the 1-5%). There are several hypotheses to explain the disease causes, try. The treatment is currently more than the drug at an affordable price, the holinèrgičeskie, which suggests that this position reduces the synthesis of acetylcholine as a neurotransmitter. Holinèrgičeskie-hypothesis is supported by a wide range of support, including management of drugs was not a very effective acetylcholine deficiency. Other effects have been proposed, such as aggregation, neuro-inflammation, the principle of universal holinèrgičeskie busters.

The control provides the beta-amyloid bearings (which are Aβ) in 1991, the year of the disease hypothesis tests are the main reason. In support of this hypothesis comes from the gene, chromosome 21, but people trisomia 21 (down syndrome), the protein amyloid-beta precursor protein (APP), the location of the extra copy of the gene, nearly all of the more than 40 years after the exhibition. ApoE4 genetic risk factor is the basic ad leads to a buildup, brain busters. Other evidence leads to the conclusion, in the form of a mutant gene in the transgenic mice expressing to develop fibrillar amyloid APP of Alzheimer's disease and the popular party spatial learning deficits. the brain pathology Committee

An experimental vaccine to amyloid plakkoknak delete the first experiments was found, but does not have a significant effect on dementia. Scientists suspect and Aβ oligomers (aggregates of many monomers) as the primary vector of shape of Aβ. These toxic amyloid oligomers derived neural circuit of synapses and neurons is superficial and opponents events to change the structure of a diffusible ligands (ADDLs) connected. The antidote, which are Aβ oligomers can prionovyh same protein linked to mad cow disease, the Krejtcfel "Yes-Jakob disease, a potentially basic neuro-degenerative diseases, and mechanisms of Alzheimer's disease." human understanding of protein

in 2009, the beta-amyloid protein has been updated, the theory is not necessarily a nearby, and amyloid beta-is the disease may be the main culprit. The theory considers that nerve cells during the early stages of life and remove links may cause the underlying mechanism of brain Busters, aging process, which would later be strong in life, that Neuronal outbreaks of the disease. N-APP, movie, N-terminal beta-amyloid peptide, exfoliado and enzymes the same APP. N-APP, the median nerve by reference to the beneficiary shall be determined by the receptor 6 (DR6, also known as TNFRSF21) dead. DR6 is highly expressed in the brain affected by Alzheimer's disease, so it is possible, using N-APP Central brain of aging damage DR6. This document template package in Synaptic beta amyloid-services export.

the investigation revealed that deposition of amyloid plaque in 2004, the correlation is not a loss of nerve. This observation disorders of protein Tau Tau hypothesis, the idea is supported by the disease cascade. In this model, the roads to other Tau Tau begins along fibres. At the end of the nerve cells of the body in the form of problems. If this happens, Disintegrate, the neuron's transport system collapsing mikrotubuly. First, you may cause interference, neurons, and the cell death of biochemical communication.

Viruses herpes simplex type 1, also known as version of the apoE gene, the causal role in sensitive individuals.

Charges against this disease spôsobené starnutím Inú Myelín time the collapse of bone marrow. Myelín the Chair rail, the exhaustion of the damage we. Myelín rozvoju vkladov bielkovinového napomáhajú patch if amyloid beta, Tau homeostatic process.

Oxidative stress and metabolic Homoeostasis biometal (Biology), i.e. the formation of pathology may be important.

Notices of individuals, 70% cell loss Noradrenaline locus (in his role), which "rotary" endogenous nerve cells, neurons, and distracts the environment micro blood vessels cortex and hippocampus cells desensitizing agent. Norepinephrine and microglia Aβ and phagocytosis in mice induced by cytokines suppress production stimulates