Current Understanding of the Physiopathology, Diagnosis and Therapeutic Approach to Alzheimer's Disease
No Thumbnail Available
Identifiers
Date
2021-12-01
Authors
Garcia-Morales, Victoria
Gonzalez-Acedo, Anabel
Melguizo-Rodriguez, Lucia
Pardo-Moreno, Teresa
Costela-Ruiz, Victor Javier
Montiel-Troya, Maria
Ramos-Rodriguez, Juan Jose
Advisors
Journal Title
Journal ISSN
Volume Title
Publisher
Mdpi
Abstract
Alzheimer's disease (AD) is the most common cause of dementia. It is characterized by cognitive decline and progressive memory loss. The aim of this review was to update the state of knowledge on the pathophysiological mechanisms, diagnostic methods and therapeutic approach to AD. Currently, the amyloid cascade hypothesis remains the leading theory in the pathophysiology of AD. This hypothesis states that amyloid-beta (A beta) deposition triggers a chemical cascade of events leading to the development of AD dementia. The antemortem diagnosis of AD is still based on clinical parameters. Diagnostic procedures in AD include fluid-based biomarkers such as those present in cerebrospinal fluid and plasma or diagnostic imaging methods. Currently, the therapeutic armory available focuses on symptom control and is based on four pillars: pharmacological treatment where acetylcholinesterase inhibitors stand out; pharmacological treatment under investigation which includes drugs focused on the control of A beta pathology and tau hyperphosphorylation; treatment focusing on risk factors such as diabetes; or nonpharmacological treatments aimed at preventing development of the disease or treating symptoms through occupational therapy or psychological help. AD remains a largely unknown disease. Further research is needed to identify new biomarkers and therapies that can prevent progression of the pathology.
Description
MeSH Terms
DeCS Terms
CIE Terms
Keywords
Alzheimer's disease, senile plaques, beta-amyloid protein, tau protein, diagnosis, biomarker, treatment, acetylcholinesterase inhibitors, immunotherapy, Cerebral amyloid angiopathy, Mild cognitive impairment, Insulin-degrading enzyme, National institute, Association workgroups, Plaque-formation, Transgenic mice, Risk-factors, Mixed-model, Mouse model