The “Fake” Alzheimer’s Study: 5 Things to Know
- Alzheimer’s facts and figures
- “Fake” research
- #1. What exactly did Lesné “fake”?
- #2. Who exposed him?
- #3. Can we reject Aβ*56 as a marker for AD?
- #4. Are we back to square one?
- #5. What markers are currently being used in the diagnosis of AD?
- Cutting Edge: AD could be predicted up to 15 years before onset!
Alzheimer’s is a brain disease that is progressive, meaning that as time goes on, the disease gets worse. What is interesting about Alzheimer’s is that it begins to manifest itself 20 years or more before symptoms arise. During this time, the structure of the brain slowly begins to change and nerve cells (neurons) in parts of the brain that are involved in thinking, learning, and memory (cognitive function) become damaged or destroyed.
Eventually, neurons in parts of the brain that allow a person to carry out basic bodily functions, such as swallowing and walking are affected, and as a result, individuals become bed-bound and require continuous care. Alzheimer’s disease is ultimately fatal.
Alzheimer’s facts and figures
It is estimated that around 6.2 million Americans aged 65 years and older are living with Alzheimer’s dementia today.1 This number is expected to grow to 13.8 million by the year 2060 unless a medical breakthrough is developed to prevent, slow, or cure Alzheimer’s disease (AD). Official death certificates recorded 121,499 deaths from AD in the US in 2019, making Alzheimer’s the sixth-leading cause of death in the United States and the fifth-leading cause of death in Americans aged 65 years and older.1 Between 2000 and 2019, deaths from heart disease, stroke, and HIV decreased, whereas deaths from AD increased by more than 145%.
See also: Can a ketogenic diet help prevent Alzheimer’s?
AD is still a huge medical issue, not just in the United States, but worldwide. Research is ongoing and great effort is being made to understand how and if it can be detected early, as well as if certain ‘markers’ can be used to detect AD early on in the disease. One of these markers, namely Aβ*56, or “amyloid beta star 56” was discovered by Sylvain Lesné, a neuroscientist and associate professor at the University of Minnesota. His work developed a leading theory that stated that the amyloid beta protein formed sticky plaques in the brain that were the main cause of Alzheimer’s. His work suggested that Aβ*56 was the cause of memory loss…until now.
Lesné has been accused of fabricating2 a key section of a 2006 study of Alzheimer’s disease3. Incredibly, Science (a prestigious scientific/medical journal) said it found more than 20 “suspect” papers by Lesné and identified more than 70 instances of image tampering in his studies. The scientific community has been rocked by these allegations and questions as to whether the results from this work should be trusted is currently being discussed.
See also: What is the best diet for preventing Alzheimer’s?
Let’s dig a little deeper into this “fake” research and discuss some key points that you should know.
#1. What exactly did Lesné “fake”?
Well, after carefully scrutinizing images that Lesné had included in his papers, it was clear that those images showing the presence of Aβ*56 looked to have been selectively ‘enhanced’, meaning brightened. By doing this, he ‘proved’ that this protein was expressed in images from AD patients or mouse models.
#2. Who exposed him?
Dr. Matthew Schrag, a neuroscientist at Vanderbilt University was the whistle-blower and raised concerns last year about the possible image manipulation in multiple papers by Lesné. It was also an issue that other scientists failed to replicate these findings in their own laboratories-which is normally a huge red flag. Dr. Thomas Wisniewski who is a professor of neurology at the New York University Alzheimer’s Disease Center told NBC news2 that Aβ*56 had never been observed in his work on AD.
#3. Can we reject Aβ*56 as a marker for AD?
Well, this is difficult to say because recent studies have found Aβ*56 in the nasal discharge of mild AD patients4 and animal models of ageing5. Based on this, it appears that Aβ*56 does have its place in AD but its role in the brain, as Lesné stated, is still under scrutiny.
#4. Are we back to square one?
Despite these findings being a potential setback, and although a re-evaluation on Aβ*56 as a marker of AD needs to be done, we’re not back to square one. From the time of this study in 2006, hundreds of papers have been published that have presented several other key biomarkers that show promise in their role in contributing to AD development.
#5. What markers are currently being used in the diagnosis of AD?
Despite the work of Lesné allegedly being fake, his work prompted researchers to look at other Aβ species and determine their role in AD progression or diagnosis.
Aβ42, the most toxic form of the Aβ, can be measured in the cerebrospinal fluid of AD patients and allows the identification of AD in its preclinical (pre-symptom) stage. It has a high diagnostic value, with clear specificity for AD over other neurodegenerative diseases. The ratio between Aβ42/Aβ40 has shown promise as a predictor of AD in several studies. This has led to the development of the Lumipulse G β-Amyloid Ratio (1-42/1-40) test that was recently permitted by the U.S. Food and Drug Administration to start the marketing process.6 This is the first diagnostic test for the early detection of AD in adult patients aged 55 years and older presenting with AD symptoms. It promises same-day results and is said to provide the same information as a PET scan, but without the risk that comes with radiation.
People carrying the APOE4 allele are at high risk of AD and this is because ApoE has a central role in controlling the transport of brain lipids(fats), neuronal signaling, energy metabolism, and neuroinflammation. What is interesting is that ApoE acts as the main cholesterol carrier protein that increases Aβ production during AD.7 ApoE has shown strength as a biomarker for AD pathogenesis since the ApoE ɛ4 allele is the strongest genetic risk factor for AD. Measurements of ApoE protein levels in cerebrospinal fluid have been performed in relation to the diagnosis of AD and are currently being assessed for its efficacy.8
Cutting Edge: AD could be predicted up to 15 years before onset!
If you can recall, I mentioned that Alzheimer’s begins to manifest itself 20 years or more before actual symptoms arise. Well, together with this, researchers have found that certain health conditions are significantly associated with the development of AD up to 15 years before the onset of the disease.
Research published in March this year conducted an agnostic study of French and British health records using data from 20 214 patients with Alzheimer’s disease in the UK and 19 458 patients with Alzheimer’s disease in France.9 This huge scientific undertaking found that symptoms appearing at least 9 years before the first clinical diagnosis was depression, which was the first comorbid condition associated with Alzheimer’s disease, followed by anxiety, constipation, and abnormal weight loss. This study brings to light that these risk factors and early signs of AD that are observable at the general practitioner level could guide the implementation of preventative measures to slow down the development of AD in individuals at risk!