ABSTRACT
Introduction: Alzheimer’s disease (AD) is a slow, irreversible, progressive, complex, and fatal neurodegenerative disorder. Available pharmacological treatment, known for almost two decades, does not cure the disease, but only alleviates the symptoms, with various efficacy and different side effects. Therefore, there is an unmet need to find other person-centered or personalized approaches to treat AD.
Areas covered: This article describes the application of precision medicine-like approaches utilizing nonpharmacological treatment strategies and the use of natural products in personalized care for patients with AD.
Expert opinion: Due to the heterogeneity of disease symptoms, somatic conditions, and patient preferences, there is definitely no “one size fits all“ intervention. Therefore, individualized treatment choice is based on dementia stage, medical and psychiatric comorbidity, leading symptoms, patient preferences, and remaining capacity of the patient. In the absence of disease-modifying agents, a patient-centered, multidisciplinary team approach appears to be the best option to alleviate the heavy symptomatic burden in this unfortunate population. Hence, appropriate interventions can be offered along the AD continuum, while a better understanding of personal characteristics might help in establishing optimal individualized treatment, as well as its duration and intensity, to deliver interventions in the most effective ways.
Article highlights
Personalized treatment interventions (nonpharmacological treatment and effects of natural products) in Alzheimer’s disease (AD) are described
Current pharmacological treatments do not cure or stop AD
Use of physical activity, acupuncture, animal-assisted, bright light, horticultural, music, visual art, and massage therapy might improve behavioral symptoms in AD
Natural products and vitamins improve the effectiveness of existing AD treatments
Combination of pharmaco- and nonpharmacological treatments and natural products might offer person-centered approaches to treat AD
Abbreviations
Aβ, amyloid beta; ACh, acetylcholine; AChE, acetylcholinesterase; AD, Alzheimer’s disease; ApoE, apolipoprotein e; ABCA1, ATP-binding cassette transporter G-1; BACE-1, β-site amyloid precursor protein cleaving enzyme-1; BDNF, brain-derived neurotrophic factor; CBD, Cannabidiol; COX-2, cyclooxygenase 2; CSF, cerebrospinal fluid; GABA, gamma aminobutyric acid; GDNF, glial cell-derived neurotrophic factor; GSK-3b, glycogen synthase kinase-3b; IL, interleukin; iNOS, inducible nitric oxide synthase; JNK, c-Jun N-terminal kinase; LRP1, lipoprotein receptor-related protein 1; MAO, monoamine oxidase; MCI, mild cognitive impairment; NFκB, nuclear factor kappa B; NGF, neural growth factor; NMDA, N-methyl-D-aspartate; NFT, neurofibrillary tangles; PI3K, phosphoinositide 3-kinase; RAGE, receptor for advanced glycation end products; RNS reactive nitrogen species; ROS, reactive oxygen species; Sirt-1, sirtuin 1; THC, Δ9-tetrahydrocannabinol; TNF1α, tumor necrosis factor alpha; Trk, tropomyosin-related kinase A
Acknowledgments
The authors are grateful to Milka Sagud, MSN, PMHNP, a native English speaker, for correcting the English language.
Declaration of interest
The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or conflict with the subject matter or materials discussed in this manuscript apart from those disclosed.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.