ISLAMABAD, Jan 17 (Online): Approximately 32 million peopleTrusted Source around the world have Alzheimer\u2019s disease, a type of dementia causing memory loss and other types of cognitive issues.
\nThere is currently no cure for Alzheimer\u2019s disease, and researchers are still not completely sure what causesTrusted Source the condition. There are some medicationsTrusted Source available to help treat symptoms and potentially slow the progression of the disease.<\/p>\n
Now, researchers from Amsterdam University Medical Centers and Maastricht University in the Netherlands have identified five biological variants directly related to Alzheimer\u2019s disease.
\nScientists believe these findings \u2014 recently published in the journal Nature AgingTrusted Source \u2014 may impact how future Alzheimer\u2019s treatments are developed and prescribed.<\/p>\n
Why look for Alzheimer\u2019s biological variants?
\nAlthough researchers do not know the exact cause behind Alzheimer\u2019s disease, most agree the formation of beta-amyloid plaque build-upTrusted Source and tau tanglesTrusted Source characterize it.
\nDr. Betty Tijms, associate professor of neurology, brain imaging, and neurodegeneration at Amsterdam University Medical Centers and lead author of this study, told Medical News Today that she and her team decided to look for biological processes other than beta-amyloid and tau that may affect Alzheimer\u2019s disease.<\/p>\n
They did that because genetic and tissue proteomic studies previously pointed out that other biological processes beyond amyloid and tau seem to be involved in Alzheimer\u2019s disease.
\n\u201cBut this was difficult to study in patients because the brain is not easily accessible,\u201d Dr. Tijms continued. \u201cNew techniques made it possible to measure many proteins in the cerebrospinal fluidTrusted Source, and the levels of those proteins provide a detailed picture of the processes that are ongoing in the brain.\u201c<\/p>\n
\u201dSo we made use of these innovations to study if certain subgroups of Alzheimer\u2019s disease patients could be identified that share distinct underlying biological processes,\u201d she added.
\nWhat are the 5 biological variants of Alzheimer\u2019s disease?
\nFor this study, Dr. Tijms and her team examined a little over 1,000 proteins in the cerebrospinal fluid of 419 people with Alzheimer\u2019s disease. Through this examination, they discovered five biological variants within this group.
\nAccording to Dr. Tijms, the first subtype was characterized by abnormal outgrowth of nerve cells.<\/p>\n
She explained:
\n\u201cOutgrowth is a normal process in the brain when connections between nerve cells get damaged, for example, because of the clumping of amyloid-beta. But here we see that this process goes into overdrive, and does not seem to efficiently repair the connections. The immune system of this variant was not activated properly, which may [interfere] with the clearance of protein clumps.\u201d<\/p>\n
\u2013 Dr. Betty Tijms
\n\u201cThe second subtype had an overactive immune system, which aggravated the disease progression,\u201d Dr. Tijms continued. \u201cThe third subtype had problems with the synthesis of proteins \u2014 RNA metabolism dysfunctionTrusted Source.\u201d
\n\u201dThe fourth subtype had damage in the choroid plexusTrusted Source, which is the organ in the brain that produces cerebrospinal fluid,\u201d she said. \u201d[And] the fifth subtype showed leakage of the blood-brain barrier.\u201d<\/p>\n
Surprising results may impact drug development
\nBoth researchers found some of the discovered Alzheimer\u2019s disease biological variants surprising.
\n\u201cI was surprised by the subtype with dysregulated RNA metabolism because such processes have not been highlighted as a key factor in Alzheimer\u2019s disease,\u201d Dr. Pieter Jelle Visser, professor of molecular epidemiology of Alzheimer\u2019s disease at Maastricht University in the Netherlands and senior author of this study, told MNT.<\/p>\n
\u201cIt was surprising to see the new subtype with choroid plexus dysfunction,\u201d Dr. Tijms also noted. \u201cThey had similar effects as [the] blood-brain barrier with low cerebrospinal fluid tau levels, for example, but no indication at all of leakage of blood proteins in the cerebrospinal fluid.\u201c
\n\u201cTo me that indicates that these brain interfaces are really two different entities, with their own roles in Alzheimer\u2019s disease,\u201d she told us.<\/p>\n
Both researchers believe these findings may change how Alzheimer\u2019s medications are developed and prescribed in the future.
\n\u201cThe existence of these subtypes suggests that each subtype may need a different treatment,\u201d Dr. Visser explained. \u201cFuture trials should take this into account and test their treatment in the subtypes that matched with the working mechanism of the drug.\u201d
\n\u201cAlternatively, each future Alzheimer\u2019s disease trial should stratify on subtypes such that the subtypes that best respond to treatment can be identified,\u201d he added. \u201cFuture trials may also take into account that side effects may differ between subtypes as well.\u201d
\nPotential to accelerate intervention research
\nAfter reviewing this study, Dr. Karen D. Sullivan, a board-certified neuropsychologist, owner of I CARE FOR YOUR BRAIN, and Reid Healthcare Transformation Fellow at FirstHealth of the Carolinas in Pinehurst, NC, told MNT she found this research to be extremely hopeful, as it has been known for a long time that Alzheimer\u2019s disease is an extremely heterogeneous subtype of neurodegenerative diseaseTrusted Source.<\/p>\n
\u201cSome patients have a slow and steady decline while others progress quickly,\u201d she continued. \u201cSome have predominantly memory symptoms while others experience primarily visual and spatial impairments. Identifying these five specific disease processes in Alzheimer\u2019s disease is a necessary starting point [for] personalizing brain healthcare interventions.\u201d<\/p>\n
Dr. Jennifer Bramen, a senior research scientist at the Pacific Neuroscience Institute in Santa Monica, CA, also not involved in the current study agreed, saying: \u201cThere are many known risk factors for Alzheimer\u2019s disease, and each patient has a unique risk profile. Patients exhibit diverse symptoms, progression timelines, and neurodegeneration patterns.\u201d
\n\u201cIf the authors are correct in their hypothesis that different Alzheimer\u2019s disease variants may respond differently to treatments, there\u2019s an opportunity to reassess drugs that showed promise in earlier research but were not effective overall. If true, this has the potential to accelerate intervention research.\u201d<\/p>\n
\u2013 Dr. Jennifer Bramen
\nFor the next steps in this research, Dr. Sullivan said she would like to see researchers find out if these five biological variants result in distinct clinical syndromes in people living with Alzheimer\u2019s disease.
\n\u201cWhat is the specific set of cognitive and behavior symptoms and the prognostic significance of these five variants \u2014 is there a cause-and-effect relationship?\u201d she continued. \u201c[And] the ultimate question \u2014 and here is where the hope lies \u2014 do these five variants respond preferentially to different experimental drugs or from different types of preventative or early interventions that keep the disease process from spreading throughout the brain?\u201d<\/p>\n","protected":false},"excerpt":{"rendered":"
ISLAMABAD, Jan 17 (Online): Approximately 32 million peopleTrusted Source around the world have Alzheimer\u2019s disease, a type of dementia causing memory loss and other types of cognitive issues. There is currently no cure for Alzheimer\u2019s disease, and researchers are still not completely sure what causesTrusted […]<\/p>\n
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