2020
DOI: 10.1002/ddr.21652
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Alzheimer's disease: A need for personalized therapeutic approaches

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Cited by 6 publications
(5 citation statements)
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“…For example, atherosclerosis or cardiac dysfunction may appear in one AD patient but be absent in another. As Frenkel (2020) noted, there is the potential of an “arsenal of drugs that can be used to personalize medicine for each patient in the spectrum of diseases associated with AD” [ 118 ]. This approach, however, still faces many challenges, such as determining which “cocktail” of drugs to use and how drugs interact with one another, but nanotechnological constructs offer one possible route to personalize therapeutic protocols.…”
Section: Discussionmentioning
confidence: 99%
“…For example, atherosclerosis or cardiac dysfunction may appear in one AD patient but be absent in another. As Frenkel (2020) noted, there is the potential of an “arsenal of drugs that can be used to personalize medicine for each patient in the spectrum of diseases associated with AD” [ 118 ]. This approach, however, still faces many challenges, such as determining which “cocktail” of drugs to use and how drugs interact with one another, but nanotechnological constructs offer one possible route to personalize therapeutic protocols.…”
Section: Discussionmentioning
confidence: 99%
“…However, AD is not solely attributed to a single factor like AChE inhibition; instead, it is a multifactorial condition. Factors like oxidative stress, neuroinflammation, neurotransmitter imbalance, and mitochondrial and synaptic dysfunction are also key contributors to cognitive decline [ 8 , 9 ]. Consequently, the most effective therapy for AD should be able to influence the disease via multiple pathways rather than targeting a single dysregulated mechanism.…”
Section: Introductionmentioning
confidence: 99%
“…At present, there are no effective treatments. While much emphasis has been given to the amyloid and tau proteins, multiple factors are involved in the causation of AD, including mitochondrial dysfunction, oxidative stress, unbalanced iron metabolism, and neuroinflammation [ 2 , 3 ]. Consequently, treating the end result of the disease, such as focusing on amyloid beta (Aβ) peptides or tau phosphorylation, has not yielded satisfactory results.…”
Section: Introductionmentioning
confidence: 99%