An Alzheimer’s drug cut expected cognitive decline roughly in half. It didn’t target amyloid

 You may need this; do you have a competent? doctor ready?

Your risk of dementia, has your doctor told you of this?  Your doctor is responsible for preventing this! Is s/he willing to prevent this?

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

The latest here: 

An Alzheimer’s drug cut expected cognitive decline roughly in half. It didn’t target amyloid

Researchers say the oral drug LM11A-31 slowed the decline of brain-network function in a small trial, pointing to a potential broader strategy for treating Alzheimer’s.

Could the key to treating Alzheimer’s be protecting the brain’s wiring? Potentially.

Last month, at the Alzheimer’s Association International Conference in London, Indiana University and the biopharmaceutical company PharmatrophiX presented findings that an oral drug called LM11A-31 slowed the decline of brain-network function in people with mild-to-moderate Alzheimer’s. The results, which were drawn from brain scans of 159 trial participants, point to a treatment strategy that looks well beyond the field’s longtime focus on amyloid, according to a press release.

For years, most Alzheimer’s drug development has centered on clearing amyloid plaques, and more recently tau tangles. But researchers say it’s more complicated than that.

“The main reason [to look further] is that pure amyloid beta plaque and tau tangle Alzheimer’s disease is rare,” Maria C. Carrillo, chief science officer at the Alzheimer’s Association, told Inc. The association awarded PharmatrophiX a $600,000 grant in 2013 to run an early safety trial of the oral drug LM11A-31. 

In most biologically confirmed cases, she told Inc., it’s actually “mixed dementia,” with other proteins and vascular damage present alongside the two hallmark lesions. That complexity is pushing scientists toward treatments that protect the brain itself. 

“Alzheimer’s is a complex disease driven by multiple interacting mechanisms,” Aaron Burstein, head of search and evaluation at the Alzheimer’s Drug Discovery Foundation, told Inc. The foundation has backed the drug’s lead inventor, Frank Longo, since 2000 and was an early investor in PharmatrophiX. 

“Amyloid is a validated target, but it is unlikely to be the only one,” he said.

The oral drug LM11A-31 focuses on the synapses, the junctions where brain cells communicate. It targets a receptor called p75, and according to the release, earlier studies have suggested it can make synapses more resilient to the damage caused by both amyloid and tau.

The new part is the ability to measure whether that’s actually working. The Indiana University team, led by Paul Territo, processed metabolic PET scans to build “network maps” of how efficiently different brain regions communicate.  Related video: Groundbreaking Alzheimer's treatment offers patients new hope (FOX 35 Orlando) 

“Alzheimer’s disease is not simply a disease of individual brain regions. It is a disease of disrupted brain networks,” Territo said in the release.

The analysis found dose-dependent effects, with the strongest benefits in patients on the higher 400-milligram dose, along with distinct patterns between men and women. It builds on earlier results, in which the drug cut the expected progression of cognitive decline roughly in half.

“Protecting synapses has become a central therapeutic goal,” Burstein told Inc. “This type of approach could support a precision medicine framework in which treatments target different aspects of the disease and are ultimately combined based on each patient’s biology.”

Implications for the future of Alzheimer’s treatments

Everyone involved has been careful to call the signal a starting point.

“LM11A-31’s potential will need to be confirmed in a larger clinical trial,” Burstein said. 

Investors, clinicians, and patients, he added, will want consistent evidence that the drug slows cognitive and functional decline in ways that are meaningful in daily life and sustained over time.

Carrillo agreed that the next step runs through regulators. She said that confirming the signal means a trial showing that over one to two years the treatment “slows or perhaps even stops the memory decline in comparison to a placebo group,” on terms agreed upon with the FDA.

In the release, PharmatrophiX said more planning is underway for that larger Phase 2b/3 trial. If it succeeds, LM11A-31 could become one more tool used alongside amyloid drugs.

“We know that the current approved treatments for early Alzheimer’s disease are just the beginning,” Carrillo told Inc. “More treatments are coming, each improving on the earlier treatments.”

PharmatrophiX did not respond to Inc.’s request for comment. 

This post originally appeared at inc.com.

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