Basic Sciences and Clinical Implications of Alzheimer’s Disease Volume 3 - Issue 2

Monica Fernandes Gomes*

• Associate Professor and Researcher, Center of Biosciences Applied to Patients with Special Health Care Needs (CEBAPE) at the Institute of Science and Technology, Campus of São José dos Campos, São Paulo State University–UNESP, São Paulo, SP, Brazil.

Received:June 12, 2021   Published: June 18, 2021

Corresponding author: Monica Fernandes Gomes, Institute of Science and Technology, Campus of São José dos Campos, São Paulo State University–UNESP, São Paulo, SP, Brazil.E-mail:monica.gomes@unesp.br

DOI: 10.32474/JCCM.2021.03.000157

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Abstract

Alzheimer’s disease (AD) is an irreversible and chronic progressive neurodegenerative disorder characterized by progressive cognitive dysfunction, memory loss, and decline. This disorder is the most common dementia type in elderly, accounts for 60%-80% of all cases [1-4]. Current estimates described that about 50 million people are living with dementia worldwide and treatment options are limited, placing significant suffering and financial burden on families and society. This number of people with dementia is predicted to increase to 131.5 million by 2050, as the population ages [4,5]. Although the AD etiology is still unknown, certain risk factors may influence on the clinical course of this illness, such as: age, gender, ethnicity, expression of the epsilon4 allele of apolipoprotein E (ApoE4), advanced parental age, cerebrovascular disease, severe or repeated head trauma, hypertension, myocardial infarction, diabetes mellitus, hyperlipidemia, and immunological defects; genetic factors as chromosomal defects (e.g., Down syndrome); and environmental factors as infective agents, toxins, smoking, elitism, limited education resulting in low neurofunctional stimulation, and sedentary lifestyle. Despite some controversies, authors report that limited education can be related to the high incidence of AD, once low neurofunctional stimulation could result in less cerebral metabolism and, as a consequence, favor the β-amyloid peptide (Aβ) deposits in the brain [1,6-8]. About 1% of cases of AD is autosomal dominant inheritances which is caused by high penetrance mutations in three genes, including APP (amyloid precursor protein, chromosome 21), PSEN1 (Presenilin 1; chromosome 14) and PSEN2 (Presenilin 2; chromosome 1) genes. The presence of the ApoE gene, located on the long arm of chromosome 19 (locus 19q13.2), increases the risk of developing AD. Among the three common ApoE allelic forms (epsilon2, epsilon3, and epsilon4), the ApoE4 is the most significant genetic risk factor for formation and deposition of β-amyloid peptide (Aβ) plaques in the brain tissue. These plates are neurotoxic agents which impair the synapses and ultimately cause neurodegeneration for early-onset and late-onset AD [2,3,6,8,9].

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