Alzheimer Disease

Alternative Names

  • AD
  • Presenile and Senile Dementia
  • Alzheimer Disease, Familial, 1
  • AD1
  • Alzheimer Disease, Early-Onset, With Cerebral Amyloid Angiopathy
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WHO-ICD-10 version:2010

Diseases of the nervous system

Other degenerative diseases of the nervous system

OMIM Number

104300

Mode of Inheritance

Autosomal dominant

Gene Map Locus

4p14-p13,6p22.2,7q36.1,10q22.2, 10q24,11q24.1,12p11.23-q13.12, 12p13.31,17q11.2, 17q22, 17q23.3,19p13.2,20p,21q21.3

Description

Alzheimer Disease (AD) is a progressive and fatal disease of the brain and is the most common form of dementia. The disease is characterized by progressive destruction of brain cells, resulting in serious memory, cognitive, and behavioral problems. Symptoms of AD begin slowly. Initial symptoms may be mild forgetfulness and is easily confused with age-related forgetfulness. However, as the disease progresses, the forgetfulness takes on a more serious nature, and affected people fail to recognize even close family members or caregivers, and more importantly, can forget how to perform simple daily activities. They may also have difficulties in speaking and understanding, and at times, turn aggressive and/or anxious. Patients are also prone to additional health problems, such as infections and frequent falls, mostly due to their inability to take care of themselves. Thus, affected patients need to be cared for and continuously looked after.

The most important risk factor for AD is recognized as age. Researchers have estimated that the number of affected people doubles every 5 years beyond the age of 65. In most industrialized countries, about 14% of people over 65 years of age and over 40% of people over 80 years of age are estimated to be affected with AD.

The anatomic pathology in AD is recognized as the presence of neurofibrillary tangles and senile plaques, accompanied by cerebrocortical atrophy. However, the tangles and plaques need to be present in sufficient numbers and in a characteristic distribution. A definite diagnosis of AD can only be confirmed upon autopsy of the brain tissue. Therefore, if the person is alive, only a 'probable' diagnosis of AD is possible. However, most physicians can analyse the medical history of the patient, and conduct basic medical tests, mental status evaluation, and neuropsychological tests and diagnose AD in 90% of the cases. The condition has no cure. Treatment can only be symptomatic, where certain medicines can be used to control the behavioral features of the condition. Caregivers are a very important aspect of patients' lives.

Several forms of AD have been noticed to occur in families, indicating the role of genetics in the development of the condition. The most important one is the early-onset form of AD, which occurs between the ages of 30 and 60 years. A fairly significant number of affected families worldwide have been found to carry mutations in the Presenilin-1 gene on chromosome 14. A smaller number of affected families have also been shown to carry mutations in the presenilin 2 gene on chromosome 1 or the Amyloid Precursor Protein (APP) gene on chromosome 21.

The more common version of AD, the late-onset form, does not have such a clear genetic component. It is thought that this form involves interplay of both genetic and environmental factors. The most important gene thought to be related to this form of the condition is the Apolipoprotein E (ApoE) gene. One variant of this gene, ApoE4, has been shown to be associated with an increased risk for developing AD. Interestingly, the ApoE4 variant is also a known risk factor for vascular dementia.

Epidemiology in the Arab World

View Map
Subject IDCountrySexFamily HistoryParental ConsanguinityHPO TermsVariantZygosityMode of InheritanceReferenceRemarks
104300.G.1.1Lebanon Alzheimer diseaseNM_001302688.2:c.466T>CEl Shamieh et al. 2018 78 patients with Alz...
104300.G.2.1LebanonUnknown Alzheimer diseaseNC_000011.10:g.86157598=Masri et al, 2019 Study with 59 Alzhei...

Other Reports

Algeria

Zouambia et al. (2008) used a large number of antibodies reactive with proteasome subunits and screened them on material from patients exhibiting tau- and synucleinopathies. Many antisera against proteasomal subunits (11S activator, 19S regulator ATPase/non-ATPase, and 20S alpha and beta) resulted in a distinct nuclear and/or cytoplasmic staining of the entorhinal-hippocampal area and the temporal cortex of patients with Alzheimer's disease. In particular an antibody directed against 19S regulator ATPase subunit 6b (S6b) specifically stained the neurofibrillary tangles and dystrophic neurites in AD, Down syndrome and aged nondemented controls. Real time quantitative PCR on the temporal cortex of AD patients revealed a significant increase in S6b subunit mRNA.

Palestine

Bowirrat et al. (2001) screened 821 elderly residents of an Arab community located in Wadi-Ara to study the prevalence of dementia of the Alzheimer type (DAT). An unusually high prevalence of DAT was observed in the area - 20.5% subjects aged 60 years or older. Prevalence was found to increase considerably with age, from 8% among those younger than 70 years to 51% among those 80 years or older. A higher prevalence of DAT was noted in females as compared to males. Bowirrat et al. (2000) suggested the possibility for the existence of autosomal recessive genes for Alzheimer disease in Wadi-Ara population considering the high rates of consanguinity in the area.

In 2002, a study conducted by Bowirrat and colleagues identified old age, female gender and lack of education as risk factors for the development of DAT (dementia of the Alzheimer type) in the Arab community from Wadi-Ara area. They also confirmed an association between vascular dementia (VaD), illiteracy, hypertension, and older age with the increased risk of developing DAT in patients with age related cognitive decline (ARCD). Data from the study by Bowirrat et al. (2002) on the APOE epsilon4 allele suggested that it could not explain the DAT prevalence in the Wadi Ara population.

Bowirrat et al. (2006) investigated the risk factors for depression in Arab subjects with DAT (dementia of the Alzheimer type) and VaD (vascular dementia) in Wadi-Ara. Of the 823 individuals, 168 had DAT and 49 had VaD. Depressive symptoms were present in 57% of DAT patients and 86% of VaD patients. A history of ischemic cardiovascular or cerebrovascular disease was found to be associated with a higher risk of developing depressive symptoms in DAT patients.

Qatar

Hamad et al. (2004) undertook a first-of-its-kind study in the region to determine the different sub types of dementia amongst a total of 134 Qatari patients diagnosed between 1997 and 2003. Medical history was taken from either the patients or from an informant. Dementia was defined according to the DSM IV criteria, while cognitive function was graded by a Modified Minimal Mental State Examination (MMSE). Patients with cognitive impairment were further evaluated by a neurologist or a geriatrist. Brain CT was analysed for all patients, and those with abnormal CT (35 patients) were further evaluated by brain MRI. The NINCDS/ARDA criteria were used to subtype these patients into Alzheimer Disease. AD was found in 29% of patients -14 males and 25 females with a mean age of 72 years. The Clinical Dementia Rating Scale (CDRS) was found to be severe in 72%, and moderate in 20%. Interestingly, 14% of these patients were hypertensive, 41% were diabetic, and 18% were both. This pattern of increased AD as compared to Vascular Dementia (VaD; 29% as opposed to 22%) was thus, similar to those reported from developed countries. In addition, AD was found to be present in conjunction with VaD in 15% of the patients. Hamad and colleagues (2004) suggested that the high prevalence of these cardiovascular risks could be the reason for the high incidence for the mixed cases of both AD and VaD.

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