The blood test, known as the Lumipulse G pTau 217/β-Amyloid 1-42 Plasma Ratio, can be used to detect amyloid plaques associated with Alzheimer’s in people ages 55 and older who have signs and symptoms of the disease, the agency said…
The test results were validated against amyloid PET or CSF tests and showed a 91.7% positive predictive value and 97.3% negative predictive value. Less than 20% of the 499 patients tested received an indeterminate result…
“Importantly, the Lumipulse G pTau217/ß-Amyloid 1-42 Plasma Ratio is not intended as a screening or stand-alone diagnostic test and other clinical evaluations or additional tests should be used for determining treatment options,” the FDA said… [end quote]
This is an important advance. Many conditions can cause neurocognitive disorders. Some people have mental decline due to interactions between their prescription drugs.
If a patient presents with neurocognitive decline the only current definitive tests for Alzheimer’s Disease (AD) are a PET scan or spinal tap, which are both invasive and expensive. A simple blood test can rule AD in or out.
Given the widespread and growing numbers of AD patients this new test could have Macro impact. 10% of people aged 65 and older have Alzheimer’s, and that by 2050 that number is expected to double.
Wendy
Certainly…if there was such a medication that could clear amyloid. That’s the holy grail. The meds that have been tested have a minimal to zero effect. They are expensive but not effective.
Wendy
The findings suggest – for the first time in a clinical trial – that early treatment to remove amyloid plaques from the brain many years before symptoms arise can delay the onset of Alzheimer’s dementia.
There was a article a while back saying that by age 85, 40% of the cohort will have some form of dementia, Alzheimer’s or other cognitive impairment requiring assistance and care.
You are right that the new blood test for Alzheimer’s would be very helpful to indicate whether a patient is beginning to develop amyloid pathology in order to start treatment before symptoms begin.
This would be especially useful for people who have dementia in their family. The blood test isn’t designed to be a screening test but it would be usefully targeted to people who are likely to have genetic mutations which would respond to the anti-amyloid drug.
Not all dementia is Alzheimer’s. The 2024 report of the Lancet Commission on dementia prevention, intervention, and care adds compelling new evidence that untreated vision loss and high LDL cholesterol are risk factors for dementia. Overall, around 45% of cases of dementia are potentially preventable by addressing 14 modifiable risk factors at different stages during the life course.
My MIL had that test a few months ago. Because it was still experimental it wasn’t covered by insurance, but we figured it was worth because it was much less invasive.
She has some form of dementia but not Alzheimer’s as it turns out.
I remember the news, sometime in the last year, reporting on a study one one of the amyloid clearing drugs that, while it cleared the plaques, the patients did not recover function. That implies that the plaques do damage that is not reversed by removing the plaques.
So, the solution would be to use the drugs prophylactically, which seems to be what the study I linked above did. That study used members of a family that early onset Alzheimer’s ran rampant in. iirc, the study showed 100% of the control group developed Alzheimer’s, while only 50% of those on the treatment developed Alzheimer’s. And that was for a drug that Roche stopped development of, because it didn’t seem very effective, but it was what was available when the study started.
So, now, the blood test will be vital, as a screening tool, just like cholesterol testing is done on, seemingly, everyone, now. Catch people with high amyloid levels, and treat it, before measurable damage is done.
The so-called “amyloid hypothesis” says that Alzheimer’s disease (AD) is caused by amyloid plaques. Those are easy to see under the microscope and were characteristic. But autopsies show that some people with heavy amyloid load did not have dementia.
There are several other hypotheses for the cause of AD. Tau protein accumulation correlates better than amyloid plaques with both the timing and location of symptoms and work is in progress on a blood test for tau.
APOE-4 is the strongest genetic risk factor for Alzheimer’s disease. This is a lipoprotein that has nothing to do with either amyloid or tau.
One area of research that has gained increasing attention for its role in disease progression is neuroinflammation. Many lines of evidence indicate that the innate immune response contributes to Alzheimer’s disease. Several genes related to Alzheimer’s disease are highly expressed in the innate immune cells of the brain, the microglia. Microglia, which normally protect brain neurons, can be “flipped” and then they literally chew up synapses. Not good.
I read a whole book about microglia.
It may be possible to alter microglial activity by altering lifestyle factors that can affect the innate immune system, such as sleep, exercise, and diet.
It’s becoming clear that AD is a complex disease.
Also, from a practical and Macroeconomic standpoint, what we really need to do is reduce the incidence of dementia, regardless of cause. That includes Parkinson’s Disease, vascular dementia and several others. Improving vascular health, maintaining a healthy lifestyle, and addressing risk factors, such as diabetes and obesity would reduce the risk of expensive chronic diseases like cardiovascular disease and cancer in addition to AD.
A narrow focus on amyloid may help somewhat but the picture is more complex.
Wendy
Well, amyloid is, apparently, something we can do something about now, wrt both early detection and treatment. Anything that significantly reduces the probability of a decade in a nursing home, is probably worth the effort.
I agree with you. But it will take many years of study to determine whether the new treatment will help a significant number of the general population, most of whom do not have the specific mutation that causes early familial Alzheimer’s.