Hey you, Alzheimer’s…. Who are you?
The “hidden” side of the disease
The origins of Alzheimer’s disease
What is Alzheimer’s disease
Alzheimer’s disease is a neurodegenerative disorder with a chronic and progressive course that results in alterations of memory, behavior, and the ability to think and perform simple tasks. It represents the most common form of dementia in the elderly population in high-income countries: an estimated 55 million people are affected, a figure that is expected to increase to 82 million by 2030 to reach 152 million by 2050 [1]. The onset of this condition is rare before age 65 while it becomes more pronounced with advancing age. Globally, the WHO (World Health Organization) states that Alzheimer’s disease and other forms of dementia are the seventh leading cause of death worldwide. In Italy, about 1 million people are affected by dementia, and of these 600,000 suffer from Alzheimer’s disease.
The “4 A’s” of Alzheimer’s
Based on the main symptoms, Alzheimer’s disease can be referred to as the “4 A’s disease.” The A’s represent the following: AMNESIA (significant memory loss), AFASIA (inability to formulate and understand verbal and written messages), AGNOSIA (inability to recognize people, objects and places) and APRASSIA (inability to make simple voluntary movements). People who manifest Alzheimer’s disease often have difficulty to perform daily activities such as driving a car, cooking a meal or paying bills; they may ask the same question several times, get lost easily and lose objects. As the disease progresses, some patients may exhibit aggressive and violent attitudes.
Causes of Alzheimer’s disease
Alzheimer’s disease is named by the german neurologist Alois Alzheimer, who in 1906 diagnosed the disease in a his 51-year-old his compatriot who manifested short-term memory loss, speech and behavior problems. From a post-mortem brain analysis, the neurologist noted the presence of abnormal protein deposits (now known as amyloid plaques and neurofibrillary tangles coming from protein TAU) accompanied by cortex atrophy. The presence of these protein deposits and the loss of connections between nerve cells (neurons) are, to date, considered the main causes behind the development of the disease. At present, experts believe that the causes of the disease are not entirely clear and that a combination of various factors are at the onset of this disease: genetic familiarity, environmental factors and lifestyle. Based on the current scientific knowledge, this combination of factors would seem to alter the conformation of specific brain proteins leading to brain toxic effects. The most widely accepted hypothesis seems to involve the metabolism of the β-amyloid precursor protein (APP), which for as yet unknown reasons leads to the formation and accumulation of a neurotoxic substance (the β-amyloid peptide), in the brain, resulting in progressive neuronal death. A second hypothesis attributes the early onset of the disease (about 13 percent of cases) to inherited genetic mutations. Early onset (before age 40) is linked to gene mutationsof the following proteins: presenilin 1, presenilin 2, APP, and apolipoprotein E [2].
Mechanisms underlying the development of the disease
Risk factors
Scientists are still investigating the reasons why some patients have a higher risk to develop the disease than others. Although some of the factors that influence the onset of the disease are known, there are probably others that have not yet been identified. Among the best-known risk conditions we find: advanced age (after age 65, the probability of developing the disease doubles every 5 years), familiarity and genetic predisposition (the risk is higher when a first-degree relative has the same disease), sex (women have a higher probability, due to hormonal factors, to develop the disease), and lifestyle (sedentary lifestyle, metabolic syndrome, and smoking) [3].
Prevention and Diagnosis
Although nowadays there is no preventive measure against the development of the disease, some research suggests that certain habits can help to prevent it. Such habits include: constant physical activity and appropriate cognitive stimulation, blood pressure periodic monitoring, blood sugar and cholesterol levels. Together these strategies could bring to an improvement of brain and cognitive well-being. To properly diagnose Alzheimer’s disease, the patient undergoes neuropsychological testing and specific brain examinations such as MRI (Nuclear Magnetic Resonance Imaging) and PET (Positron Emission Tomography) [4].
SAGE test
Early detection of early signs of dementia would make faster and more effective interventions. In this regard, Ohio University, carried out a self-administered geriatric cognitive test known as the “SAGE test.” Undergo this test periodically will help our physician to promptly detect early symptoms and quickly intervene with appropriate therapies [5]. There are 4 versions of the SAGE test. The questions regarding each version are slightly different. It does not matter which version you choose, since they are all the same in terms of difficulty and therefore interchangeable.
- The test is available at the following link: https://wexnermedical.osu.edu/brain-spine-neuro/memory-disorders/sage/download-the-sage-test
- Instructions for calculating test score: https://wexnermedical.osu.edu/-/media/files/wexnermedical/patient-care/healthcare-services/brain-spine-neuro/memory-disorders/sage/italian/sage_scoringinstructions_ita_2021.pdf?rev=583f63d342924294a2d9d61e304ad11a&hash=2F5637E07CF8EA681AB69711A7DD1124
- Explanations on the score obtained: https://wexnermedical.osu.edu/-/media/files/wexnermedical/patient-care/healthcare-services/brain-spine-neuro/memory-disorders/sage/italian/sage_infosheet_ita_2021.pdf?rev=5e3b341174b04db5a102446c5313d10d&hash=693A8BDC261779A678776E86A0F01578
[1] Manafikhi R, Haik MB, Lahdo R, AlQuobaili F. Plasma amyloid β levels in Alzheimer’s disease and cognitively normal controls in Syrian population. Med J Islam Repub Iran. 2021 Feb 8;35:19 [2] Andrade-Guerrero J, Santiago-Balmaseda A, Jeronimo-Aguilar P, Vargas-RodrÃguez I, Cadena-Suárez AR, Sánchez-Garibay C, Pozo-Molina G, Méndez-Catalá CF, Cardenas-Aguayo MD, Diaz-Cintra S, Pacheco-Herrero M, Luna-Muñoz J, Soto-Rojas LO. Alzheimer’s Disease: An Updated Overview of Its Genetics. Int J Mol Sci. 2023 Feb 13;24(4):3754 [3] A Armstrong R. Risk factors for Alzheimer’s disease. Folia Neuropathol. 2019;57(2):87-105 [4] Teipel S, Gustafson D, Ossenkoppele R, Hansson O, Babiloni C, Wagner M, Riedel-Heller SG, Kilimann I, Tang Y. Alzheimer’s Disease: Standards of Diagnosis, Treatment, Care, and Prevention. J Nucl Med. 2022 Jul;63(7):981-985 [5] https://wexnermedical.osu.edu/brain-spine-neuro/memory-disorders/sage
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