In the recent period, scientists have resorted to somewhat questionable approaches while searching for effective treatments for Alzheimer’s disease. Numerous debates and even scandals have erupted surrounding the “amyloid hypothesis,” notably fueled by suspicions of key data fabrication and the controversial approval of the drug Aducanumab in the US. The Conversation portal reports on these developments.
As noted by neurobiologists, relevant research has spanned several decades, yet attempts to block or remove amyloid plaques have failed to yield truly effective therapies. This reality is pushing scientists toward seeking fundamentally new explanations for the nature of the ailment.
Researchers from the Canadian Krembil Brain Institute, building upon over 30 years of their own work, have put forward an alternative perspective. This view suggests that Alzheimer’s disease might be less of a neurodegenerative condition and more of an autoimmune pathology affecting the brain. Under this hypothesis, beta-amyloid is not a toxic byproduct but rather a normal molecule involved in the immune defense of nervous tissue.
The immune system is present in all organs, including the brain. Its activation is triggered by injuries, inflammation, or bacterial invasions. This is where the protective role of beta-amyloid becomes crucial. However, the membranes of neurons share structural similarities with bacterial membranes. Consequently, beta-amyloid may mistakenly identify the brain’s own cells as foreign intruders and initiate an attack, thereby provoking chronic inflammation and the gradual demise of neurons.
This implies that Alzheimer’s disease is a manifestation of an autoimmune process. Yet, conventional treatments for autoimmune diseases (such as steroids) are unsuitable here because the brain is exceedingly complex and vulnerable.
The scientists advocate for shifting focus towards precisely tuning the brain’s immune signaling pathways. They contend that regulating neuroinflammation, rather than simply clearing amyloid plaques, holds the potential to pave the way for novel therapeutic strategies.
Other alternative hypotheses also exist. Some attribute Alzheimer’s disease to malfunctions in mitochondria—the cell’s “power stations.” Others pinpoint the causes in chronic infections, including those originating from oral bacteria, or in the context of disruptions in the metabolism of metals like copper, zinc, and iron.
Currently, over 50 million people globally suffer from dementia, with a new diagnosis being made every few seconds. Therefore, achieving a profound understanding of this disease’s origins is of paramount importance.
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