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Review
. 2021 Dec 14;9(12):1910.
doi: 10.3390/biomedicines9121910.

Current Understanding of the Physiopathology, Diagnosis and Therapeutic Approach to Alzheimer's Disease

Affiliations
Review

Current Understanding of the Physiopathology, Diagnosis and Therapeutic Approach to Alzheimer's Disease

Victoria García-Morales et al. Biomedicines. .

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-β (Aβ) 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 Aβ 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.

Keywords: Alzheimer’s disease; acetylcholinesterase inhibitors; biomarker; diagnosis; immunotherapy; senile plaques; tau protein; treatment; β-amyloid protein.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Evolution of the prevalence of AD according to age range (adapted from Garre-Olmo et al. [10]).
Figure 2
Figure 2
Diagram of the processing routes by which the APP can be degraded, showing how the β-amyloid peptide is produced.
Figure 3
Figure 3
Consequences of tau protein hyperphosphorylation for the structure of tubulin microtubules, a classic pathology of AD.
Figure 4
Figure 4
Overview of the main treatments in the therapeutic approach to Alzheimer’s disease.

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