Alzheimer's disease is a type of dementia caused by damage of the dendrites of the brain cell. The damage is caused by Abeta (beta-amyloid) which is a starch-like kind of protein.
Alzheimer's disease can be classified as early onset and late onset Alzheimer's disease. Usually the genetic type of Alzheimer's disease starts early from 30 to 60 years of age, whereas the late onset disease shows up late in life.
Abeta is one of the antimicrobial peptides of the innate immune system. These antimicrobial peptides defend against invading bacteria, viruses, and fungi. Abeta get triggered when there is a chronic infection, such as gum infection, Epstein-Barre, diabetes, and especially yeast infection. That is because Abeta is especially effective in inhibiting Candida Albicans, the fungus that causes yeast infection. Candida Albicans can flair up when a person consumes too much sugar or uses certain antibiotics that can kill or inhibit E. coli of the intestine, thus causing the yeast to be become overpopulated.
When Abeta is triggered, this antimicrobial peptide can get trapped in the brain. This happens because of a blood brain barrier dysfunction caused by the fluid in the brain not draining out normally or not filtering out harmful matter entering the brain normally. The Abeta thus gets trapped in the brain and causes damage to the dendrites of the nerve cells of the brain. The damaged dendrites break off, clump together, and form plaques in the brain. The plagues can be seen in special MRI tests and are signs of damaged brain cells.
Below is a report case report on immunization with Abeta.
Neuropathology of human Alzheimer disease after immunization with amyloid-beta peptide: a case report.
Division of Clinical Neurosciences, University of Southampton, Southampton, UK. J.Nicoll@soton.ac.uk
Amyloid-beta peptide (Abeta) has a key role in the pathogenesis of Alzheimer disease (AD). Immunization with Abeta in a transgenic mouse model of AD reduces both age-related accumulation of Abeta in the brain and associated cognitive impairment. Here we present the first analysis of human neuropathology after immunization with Abeta (AN-1792). Comparison with unimmunized cases of AD (n = 7) revealed the following unusual features in the immunized case, despite diagnostic neuropathological features of AD: (i) there were extensive areas of neocortex with very few Abeta plaques; (ii) those areas of cortex that were devoid of Abeta plaques contained densities of tangles, neuropil threads and cerebral amyloid angiopathy (CAA) similar to unimmunized AD, but lacked plaque-associated dystrophic neurites and astrocyte clusters; (iii) in some regions devoid of plaques, Abeta-immunoreactivity was associated with microglia; (iv) T-lymphocyte meningoencephalitis was present; and (v) cerebral white matter showed infiltration by macrophages. Findings (i)-(iii) strongly resemble the changes seen after Abeta immunotherapy in mouse models of AD and suggest that the immune response generated against the peptide elicited clearance of Abeta plaques in this patient. The T-lymphocyte meningoencephalitis is likely to correspond to the side effect seen in some other patients who received AN-1792 (refs. 7-9).
PMID: 12640446 [PubMed - indexed for MEDLINE]
Explanation of the above treatise by Joe Hing Kwok Chu :
Amyloid-beta peptide: is an antimicrobial peptide. Beta-amyloid is a starch-like protein that can help eliminate infection but can also damage the healthy brain cells. Aβ (beta- amyloid) plays a key role in the cause of Alzheimer's disease. Aβ can adjust itself to a variety of environmental stressors, and is able to induce pro-inflammatory activities.
Immunization with an Abeta vaccine in mice that were genetically induced with Alzheimer's disease, reduces the age-related accumulation of beta-amyloid in the brain and associated cognitive impairment.
The researchers immunized a human patient with Abeta vaccine, using the drug called AN-1792. ( N-1792 was developed to stimulate the immune system to "recognize" and attack the amyloid plaques that are a characteristic of Alzheimer brain abnormality).
Compared to 7 un-immunized cases, it was found that despite the diagnostic sickness of the nerves/brain of Alzheimer's disease:
Findings (1)-(3) strongly resemble the changes seen after Abeta immunotherapy in mouse models of AD and suggest that the immune response generated against the peptide, elicited clearance of Abeta plaques in this patient. The T-lymphocyte meningoencephalitis is likely to correspond to the side effect seen in some other patients who received AN-1792.
Neuropil is the nervous tissue consisting of a fibrous network of nonmyelinated nerve fibers; gray matter with few nerve cell bodies; usually a region of synapses between axons and dendrites. (click here to go back)
Cerebral amyloid angiopathy (CAA) is also known as congophilic angiopathy or cerebrovascular amyloidosis. It is a disease of small blood vessels in the brain in which deposits of amyloid protein in the vessel walls may lead to stroke, brain hemorrhage, or dementia. Amyloid protein resembles a starch and is deposited in tissues during the course of certain chronic diseases. (answers.com) (click here to go back)
Microglia are any of the small neuroglial cells of the central nervous system having long processes and amoeboid and phagocytic activity at sites of neural damage or inflammation. (click here to go back)
Neurites: Any projection from the cell body of a neuron can be referred to as a neurite. This projection can be either an axon or a dendrite. The term is frequently used when speaking of immature or developing neurons, especially of cells in culture, because it can be difficult to tell axons from dendrites in that situation. (answers.com) (click here to go back)
Abeta ( beta-amyloid) plaques: are precipitations of protein lumps inside and outside the nerve cells caused by abnormal protein-protein interactions. These abnormal interactions of protein play a role in the dysfunction and death of nerve cells in diseases such as Alzheimerís disease and Parkinsonís disease . (click here to go back)
Abeta peptide vaccination prevents memory loss in an animal model of Alzheimer's disease.
Nat Med. 2003 Apr;9(4):448-52. Epub 2003 Mar 17.
A Potential Treatment for Alzheimer's disease (from Shanghai)
See explanation of γ-Secretase in Wikipedia
中國科學院上海生命科學研究院生物化學與細胞生物學研究所裴鋼院士領導的研究小組經多年研究後發現，β2腎上腺素受體被激活後，可增強γ分泌酶的活性 ，進 而能 夠增加導致阿爾茨海默病的β澱粉樣蛋白的產生。該發現揭示了阿爾茨海默病致病的新機制，並且提示β2腎上腺素受體有可能成為研發阿爾茨海默 病治療藥物 的新靶點 。11月19日，國際著名學術期刊《自然∑醫學》網絡版在線發表了這項關於β澱粉樣蛋白產生過程新機制的最新研究成果。
 Reported by Pei Gang et al of Bio-chemistry and Cell Biology Department of Shanghai Life Science Research Institute of Science Institute of China. Natural Medicine, 2007, Nov 10.
Compiler's note: Stimulating β2-adrenergic receptor increases epinephrine and norepinephrine secretion. Example of drug that stimulates β2-adrenergic receptor: Salmeterol is a long-acting β2-adrenergic receptor (β2AR) agonist commonly used in the treatment of asthma and chronic obstructive pulmonary disease. Salmeterol is one of the 2 ingredients of Advair. See some of other β2 agonists.
EEG (electroencephalogram): a graphic record of electrical activity of the brain; produced by an electroencephalograph
From reports of various studies, it can be concluded that Alzheimer's disease is caused by beta-amyloid.
See another study here: Pro-NGF Can Be Related to Its Increased Oxidative Modifications in Alzheimer Disease
Moderately increased homocysteine levels as well as decreased folate and vitamin B12
More on Abeta (beta-amyloid)
Back to causes of memory loss.
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