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Scientists have long been racking their brains to crack the mechanism behind Alzheimer\u2019s disease progression.<\/p>\n
They may have finally found a crucial clue. A research team from Heidelberg University<\/a> in Germany recently uncovered a hidden \u201cswitch\u201d that acts like a death trigger for brain cells and plays a key role in cognitive decline.<\/p>\n The study also highlighted a new, experimental drug that could block the process, opening up possibilities for more effective treatments in the future.<\/p>\n Researchers have found a hidden switch in the brain that can worsen Alzheimer\u2019s disease, while also identifying a potential way to stop it. LIGHTFIELD STUDIOS \u2013 stock.adobe.com<\/p>\n With over 7 million people over 65<\/a>\u00a0battling the degenerative disease \u2014 and the number expected to almost double by 2050 \u2014 new treatments<\/a> are constantly being explored that tackle the toxic proteins that accumulate in the brain.<\/p>\n Researchers from Heidelberg and Shandong University in China used a mouse model of Alzheimer\u2019s to examine a molecular process in the brain involving two previously studied proteins: the NMDA receptor and the TRPM4 ion channel.<\/p>\n Both are essential components: NMDA receptors help maintain cognitive function, while TRPM4 is a membrane protein that affects immune cell function and is linked to neurodegenerative disorders.<\/p>\n When TRPM4 interacts with the receptors outside synapses<\/a> where neurons connect and communicate, the result is a toxic interaction that researchers describe as a \u201cdeath complex,\u201d damaging and killing nerve cells.<\/p>\n A toxic protein interaction in the brain between two compounds could make the degenerative disease worse over time. New Africa \u2013 stock.adobe.com<\/p>\n The study found that this neurotoxic pairing appeared at much higher levels in the Alzheimer\u2019s mice compared to the healthy ones.<\/p>\n The same team had previously discovered the novel pharmaceutical compound FP802, a neuroprotective drug that prevents neurons from dying.<\/p>\n They used this drug to block the interaction between the two proteins and successfully break the deadly complex apart, which slowed the progression of the degenerative disease.<\/p>\n The effects of FP802 didn\u2019t stop there.<\/p>\n The team noted that the compound limited or entirely prevented many of the typical cellular changes from Alzheimer\u2019s, including loss of synapses and damage to mitochondria.<\/p>\n Cognitive abilities that are often affected, such as learning and memory, remained largely intact, and the hallmark amyloid beta<\/a> deposits were significantly reduced.<\/p>\n According to the researchers, this treatment notably differs from traditional methods.<\/p>\n \u201cInstead of targeting the formation or removal of amyloid from the brain, we are blocking a downstream cellular mechanism\u2026 that can cause the death of nerve cells and promotes the formation of amyloid deposits,\u201d study lead Dr. Hilmar Bading of Heidelberg said in a statement<\/a>.<\/p>\n![\"Researchers](\"https:\/\/www.europesays.com\/us\/wp-content\/uploads\/2026\/03\/1006594a08379229fa94fce4549b24dd.jpeg\"\/)
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