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Introduction to Alzheimer What is Alzheimer? Who have an Alzheimer?

There are two main types of Alzheimer namely, early-onset Alzheimer and late-onset Alzheimer.

Early-onset Alzheimer What is it? Who have it? What are the factors that influence this types of disease? What are the symptoms, signs of this disease? How can a doctor treat this disease?
Late-onset Alzheimer

In United Kingdom, 800000 people have a dementia, and the most common dementia is Alzheimer Dementia is a set of symptoms which comprises of “loss of memory, mood changes, problems with community and reasoning”. 60000 people in United Kingdom die per year attributed to dementia. One third of aged people over 95 years old have dementia. Two third of dementia patients are women (Alzheimer’s society, 2014.a). http://alzheimers.org.uk/site/scripts/documents_info.php?documentID=341

Alois Alzheimer, a German neurologist, first described Alzheimer as a physical disease affecting the brain. People with Alzheimer have a scarcity of certain vitals chemicals, which of these involve in the transmission of messages inside the brain. During the course of Alzheimer’s, protein called plaques and tangles develop inside the structure of the brain, leading to the death of brain cells. Alzheimer’s is a progressive disease, which means gradually more parts of the brain are damaged. As a result, the symptoms and impacts from Alzheimer ‘s are likely to become more severe over time (Alzheimer’s society, 2014.b). http://www.alzheimers.org.uk/site/scripts/documents_info.php?documentID=100

There are two main types of Alzheimer namely, familiar Alzheimer’s, early-onset Alzheimer’s and late-onset Alzheimer’s.

Familiar Alzheimer’s disease or FAD is a heritable disease only, passed down inside a family (Binetti, 2012). FAD is very rare, accounting for less than1 percent of all Alzheimer’s diseases, and is more common among younger people. It has a much earlier onset often in the age of 40 year old (Glass, 2012). http://www.webmd.com/alzheimers/guide/alzheimers-types http://www.alzheimer-europe.org/Dementia/Other-forms-of-dementia/Neuro-Degenerative-Diseases/Familial-Alzheimer-s-disease?#fragment-1 Mutations in three genes were assumed to cause familiar Alzheimer’s disease. First, a genetic disorder on chromosome 21 in a gene called amyloid precursor protein (APP), intervening the production of the protein amyloid. Amyloid build up in the brain is associated to Alzheimer’s. Second, a mutation on chromosome 14, named presenilin-1 accounted for the majority of FAD cases. Third, a fault on chromosome 14, presenilin-2, leads to FAD (Binetti, 2012). A person who carries one of these mutated genes has a 50 percent chance of passing it to his or her children and those who have a mutated gene will certainly develop Alzheimer’s (Alzheimer’s society, 2014.c). file:///C:/Users/1512/Downloads/alzwa_resource_rt_fs_genetics.pdf Familiar Alzheimer’s has a similarity with early-onset Alzheimer’s that the patients from both diseases are young. However, the research has shown differences between FAD patients and NF-EAD (non-familiar early-onset Alzheimer’s) patients. “Patients with NF-EAD were more likely to present with non-memory deficits, particularly visuospatial symptoms, than were FAD patients”. When aged, FAD patients were more likely to have significant headaches, myoclonus, gait abnormality and psedobulbar effect than those with NE-EAD.

Patients with NF-EAD were more likely to present with non-memory deficits, particularly visuospatial symptoms, than were FAD patients. When age, disease duration, and MMSE scores were controlled in a logistical regression model, FAD patients were more likely to have significant headaches, myoclonus, gait abnormality, and pseudobulbar affect than those with NF-EAD. In addition to a much younger age of onset, FAD patients with PSEN1 mutations differed from those with NF-EAD by a history of headaches and pseudobulbar affect, as well as myoclonus and gait abnormality on examination. These may represent differences in pathophysiology between FAD and NF-EAD and in some contexts such findings should lead to genetic counseling and appropriate recommendations for genetic testing for FAD.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3442121/