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Review
. 2022 Mar 21;12(3):460.
doi: 10.3390/life12030460.

Personalized Management and Treatment of Alzheimer's Disease

Ramón Cacabelos  1 , Vinogran Naidoo  2 , Olaia Martínez-Iglesias  3 , Lola Corzo  4 , Natalia Cacabelos  5 , Rocío Pego  6 , Juan C Carril  7
Affiliations
Review

Personalized Management and Treatment of Alzheimer's Disease

Ramón Cacabelos et al. Life (Basel). .

Abstract

Alzheimer’s disease (AD) is a priority health problem with a high cost to society and a large consumption of medical and social resources. The management of AD patients is complex and multidisciplinary. Over 90% of patients suffer from concomitant diseases and require personalized therapeutic regimens to reduce adverse drug reactions (ADRs), drug−drug interactions (DDIs), and unnecessary costs. Men and women show substantial differences in their AD-related phenotypes. Genomic, epigenetic, neuroimaging, and biochemical biomarkers are useful for predictive and differential diagnosis. The most frequent concomitant diseases include hypertension (>25%), obesity (>70%), diabetes mellitus type 2 (>25%), hypercholesterolemia (40%), hypertriglyceridemia (20%), metabolic syndrome (20%), hepatobiliary disorder (15%), endocrine/metabolic disorders (>20%), cardiovascular disorder (40%), cerebrovascular disorder (60−90%), neuropsychiatric disorders (60−90%), and cancer (10%). Over 90% of AD patients require multifactorial treatments with risk of ADRs and DDIs. The implementation of pharmacogenetics in clinical practice can help optimize the limited therapeutic resources available to treat AD and personalize the use of anti-dementia drugs, in combination with other medications, for the treatment of concomitant disorders.

Keywords: Alzheimer’s disease; anti-dementia drugs; biomarkers; cerebrovascular genomics; concomitant disorders; neurodegenerative genomics; pathogenic genes; pharmacogenomics; phenotype-modifying treatments.

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Conflict of interest statement

RC is President and stockholder of EuroEspes (Biomedical Research Center), EuroEspes Biotechnology, IABRA, and EuroEspes Publishing Co. NC is a shareholder of EuroEspes S.A. The authors have no other relevant affiliations or financial involvement with any other organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed apart from those disclosed.

Figures

Figure 1
Figure 1
ECG (upper panel) and APOE-related ECG (lower panel) in patients with Alzheimer’s disease.
Figure 2
Figure 2
Pathogenic gene variants (upper panel) and cerebrovascular risk gene variants (lower panel) associated with Alzheimer’s disease. See Table 2 and Table 3 and Abbreviations for gene identification and SNPs of risk.
Figure 3
Figure 3
Accumulation of defective pathogenic gene variants in patients with Alzheimer’s disease.
Figure 4
Figure 4
Global DNA methylation in patients with central nervous system disorders (upper panel) and APOE-related DNA methylation in patients with Alzheimer’s disease (lower panel). C: Control; AD: Alzheimer’s disease; PD: Parkinson’s disease; CVD: Cerebrovascular disorder; MD: Major Depression; SCZ: Schizophrenia and psychotic syndromes; MIG: Migraine; EPI: Epilepsy; OID: Organic Intellectual Disability.
Figure 5
Figure 5
Noradrenaline (upper panel) and serotonin levels (lower panel) in central nervous system disorders. C: Control; ANS: Anxiety; STR: Stroke; BTU: Brain tumors; ATX: Ataxia; SCZ; Schizophrenia and psychosis; MIG: Migraine; EPI: Epilepsy; AD: Alzheimer’s disease; DEP: Depression; ALS: Amyotrophic Lateral Sclerosis; VEN: Vascular encephalopathy; MS: Multiple Sclerosis; PD: Parkinson’s disease; OID: Organic Intellectual Disability; XES: Xenoestrogenic syndrome; and BTR: Brain trauma.
Figure 6
Figure 6
Frequency of defective pharmagene variants in Alzheimer’s disease and average accumulation of dysfunctional variants per patient.
See this image and copyright information in PMC

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