Cathy Miller

β-and γ-Secretase Inhibitors & Alzheimer’s Disease

Blog Post created by Cathy Miller on Aug 29, 2018

Alzheimer's disease (or AD) is by nature a disorder featuring loss of neurons in the hippocampus and cerebral cortex. In recent decades, AD has become the most common form of dementia in seniors and it’s estimated that the number of people living with dementia would exceed 65 million by 2030. This number is likely to double every 20 years. Common symptoms are erosion of memory and other cognitive dysfunctions related to language, reasoning and alike. Following cardiovascular disease, cancer and stroke, AD is now the fourth most common cause of death in industrialized nations. To halt or even stabilize the progression of this disease, intensive efforts have been made among the scientific community, yet no available drugs are found till now.

The Amyloid Hypothesis
In an effort to crystalize the pathological cause of AD, the amyloid hypothesis was first proposed over 20 years ago. According to this theory, the accumulation of Aβ within neural tissue attributes to the occurrence of AD. The imbalance between Aβ production and clearance further leads to the formation of neurofibrillary tangles. In light of this, researchers have attempted to inhibit the generation of the beta amyloid peptide through modulation of the activity of the proteolytic secretases. β-and γ-secretase inhibitors have been investigated and discussed as to whether they might be a viable therapeutic strategy for treating AD.

Therapeutic Potential of β-and γ-Secretase
Inhibition of the β-secretase and γ-secretase would block Aβ production and thus represents a promising therapeutic strategy in AD treatment. The past decade has seen tremendous research efforts toward these two types of inhibitors but as yet no successes have been made in clinical trials. The biggest reason is probably the side effects caused by this approach.

Are β-and γ-Secretase Inhibitors effective in treating Alzheimer’s Disease?
To sum up, it stills remains unknown whether targeting the secretases involved in APP processing would yield therapeutic successes as expected, after all some high profile clinical failures have called into question the viability of the amyloid hypothesis. A number of the clinical trials of AD treatments may have failed due to the patients’ being too far advanced in the disease process. So it would be better for newer trials to be targeted at patients in earlier stages of the disease. Generally, therapeutic potentials of the β-secretase inhibitors and γ-secretase inhibitors in AD research need to be further explored.


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