Abstract

The recent article by Salloway et al was interesting. 1 Interestingly, a number of new targets have been identified, which may play a potential role in decreasing the cognitive deficits seen in patients with Alzheimer’s disease (AD).
For instance, diosgenin has recently been shown to attenuate the pathological lesions in AD. It does this by activating the 1, 25D (3)-MARRS/Pdia3/ERp57 pathway. 2 Similarly, recent studies indicate that striatal-enriched protein tyrosine phosphatase (STEP) may be involved in the pathogenesis of AD. 3 Modulation of STEP may play a major role in attenuating the risk of AD. Scyllo-inositol is another new agent that decreases neuronal toxicity by promoting low-molecular-weight Aβ and neutralizing Aβ trimers. 4
Similarly, recent studies have reported the development of new inhibitors of γ-secretase function that may attenuate the progression of AD. 5 Hsp90 is another prospective target that is being considered for the treatment of AD. 6 α-synuclein is another such potential target. 7
The above examples clearly illustrate potential new targets for ameliorating the symptoms of AD and the need for further urgent research to elaborate their potential role in mitigating cognitive decline in patients with AD.
Footnotes
Declaration of Conflicting Interests
The author declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding
The author received no financial support for the research, authorship, and/or publication of this article.
