The discovery is described in Alzheimer's & Dementia: The Journal of the Alzheimer's Association.
Associations with lower, higher riskResearchers found that higher blood concentrations of molecules called branched-chain amino acids were associated with lower risk of future dementia.
One high-density lipoprotein (HDL) and one VLDL lipoprotein subclass were associated with increased dementia risk.
Diagnostic examIn the future, the Glenn Biggs Institute may investigate the feasibility of developing a diagnostic exam, such as a blood test, to assess each patient's molecular signature of dementia risk.
The altered metabolite signatures were observed years before the diagnosis of dementia when those study participants were healthy, Dr. Seshadri said.
Posts published in “Research”
The discovery is described in Alzheimer's & Dementia: The Journal of the Alzheimer's Association.
One high-density lipoprotein (HDL) and one VLDL lipoprotein subclass were associated with increased dementia risk.
Diagnostic examIn the future, the Glenn Biggs Institute may investigate the feasibility of developing a diagnostic exam, such as a blood test, to assess each patient's molecular signature of dementia risk.
###Glenn Biggs InstituteThe Glenn Biggs Institute for Alzheimer's & Neurodegenerative Diseases was announced by William L. Henrich, M.D., MACP, president of UT Health San Antonio, in September 2015.
Dr. Seshadri, internationally respected dementia research leader from Boston University, began duties Dec. 1, 2017, as founding director of the Glenn Biggs Institute.
A new study published in the journal Alzheimer’s and Dementia links high cholesterol with a lower risk of cognitive decline for people over 85 years old.
But that might not necessarily mean that having high cholesterol prevents dementia.
In other words, higher cholesterol among the very old was associated with a reduced chance for dementia.
Study participants aged 75 to 84 years old with higher late-life cholesterol texperienced a 50 percent higher risk of cognitive decline.
“Most people prior to late old age are vulnerable to the deleterious effects of total cholesterol,” Silverman explained to The Daily Meal.
H4K16ac is a key modification in human health because it regulates cellular responses to stress and DNA damage.
In addition, the team discovered an association between the location of H4K16ac changes and genetic variants identified in prior AD genome-wide association studies.
“We found that while normal aging leads to H4K16ac enrichment, AD entails dramatic losses of H4K16ac in the proximity of genes linked to aging and AD.
This finding indicates that certain normal aging changes in the epigenome may actually protect against AD and when these go awry, a person may become predisposed to AD.
Our results establish the basis for an epigenetic link between aging and AD,” the authors concluded.
Treatments targeted to enhance brain neurotrophic factor signaling could improve memory functions in Alzheimer's disease even though they don't alter brain amyloid burden, according to recent research from the University of Eastern Finland.
The enhancement of brain derived neurotrophic factor (BDNF) signaling alleviated memory impairment in Alzheimer's mouse models.
In addition, the administration of cerebral dopamine neurotrophic factor (CDNF) into brain tissue improved long-term memory in particular.
Using transgenic APP/PS1 mouse models of Alzheimer's disease with altered BDNF signaling, the research group showed that memory impairment was aggravated by reduced BDNF signaling and alleviated by enhanced BDNF signaling.
"Thus, by enhancing neurotrophic factor signaling it may be possible to improve memory functions without altering brain amyloid burden."
But the way in which molecular processes of ageing predispose people to AD, or become impaired in AD remains a mystery.
Changes to the way H4K16ac is modified along the genome in disease versus normal ageing brains may signify places for future drug development.
Because changes in H4K16ac govern how genes are expressed, the location and amount of epigenetic alterations is called the "epigenetic landscape."
This finding indicates that certain normal ageing changes in the epigenome may actually protect against AD and when these goes awry, a person may become predisposed to AD.
Publication: Dysregulation of the epigenetic landscape of normal aging in Alzheimer’s disease.
The research team also identified the mechanisms on which the protective effects of extra virgin olive oil are based.
“Brain cells of mice that had diet enriched with extra virgin olive oil had higher levels of autophagy and decreased levels of amyloid plaques and phosphorylated tau.
Known as a triple transgenic model (3xTg), animals develop three main features of the disease: memory impairment, amyloid wounds and neurofibrillary meshes.
The researchers divided the mice into two groups, one that received a diet enriched with extra virgin olive oil and another that received a diet without the olive oil.
Olive oil was introduced into the diet when the mice were 6 months old before the symptoms of Alzheimer’s disease appeared in the animal model.
"It's such that people who are making it who remain alive and who have high cholesterol are more likely to carry other factors that protect them against the bad effects of cholesterol," he explained.
"Overall, high cholesterol was associated with a bad cognitive [mental] decline, but when we look only at people who were in good cognitive health at 85, a rising cholesterol was associated with a better outcome," Silverman said.
"We don't think that having a high cholesterol becomes a good thing -- it's just that you're likely to be the kind of person for whom cholesterol doesn't matter," he explained.
Silverman doesn't think that cholesterol itself is protective against mental decline, but that other factors protect against the bad effects of cholesterol.
"We can focus specifically on those old people with high cholesterol and look for factors that protect them from cognitive decline," he said.
The authors of this new study looked at the association of cholesterol levels and cognitive functions at different age groups.
Results revealed that increased cholesterol levels since the 40’s led to an increased cognitive decline as the participant aged.
Authors warn that this study does not advocate raising one’s cholesterol during their 40’s to reduce the risk of cognitive decline.
This is because, there is a positive risk of getting dementia among the aged if they have high cholesterol levels during their 40’s.
Further high cholesterol levels do lead to an increased risk of cardiovascular disease.