A study involving 57 cognitively healthy older adults has found that those who showed decreased memory performance two years later (20 of the 57) had higher baseline levels of phosphorylated tau231 in the cerebrospinal fluid, and more atrophy in the medial temporal lobe. Higher levels of damaged tau protein were associated with reductions in medial temporal lobe gray matter. The finding may be useful in early diagnosis of Alzheimer’s disease.
Damaged protein identified as early biomarker for Alzheimer's
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Friends, family detect early Alzheimer's signs better than traditional tests
Confirming earlier research, a study involving 257 older adults (average age 75) has found that a two-minute questionnaire filled out by a close friend or family member is more accurate that standard cognitive tests in detecting early signs of Alzheimer’s.
The AD8 asks questions about changes in everyday activities:
Losing muscle mass early sign of Alzheimer’s
Previous research has found that unexplained weight loss is an early sign of Alzheimer's. Now a study involving 140 older adults (60+), of whom half had early-stage Alzheimer's disease, has revealed that it is not the overall weight or fat levels that are important, but the loss of lean mass (weight of an individual's bones, muscles and organs without body fat). This directly correlated with reductions in the volume of the whole brain and of white matter only, along with declines in cognitive performance.
Specific hippocampal atrophy early sign of MCI & Alzheimer's
A three-year study involving 169 people with mild cognitive impairment has found that those who later developed Alzheimer's disease showed 10-30% greater atrophy in two specific locations within the hippocampus, the cornu ammonis (CA1) and the subiculum.
Loss of smell may predict early onset of Alzheimer's
Previous research suggesting loss of smell function may serve as an early marker of Alzheimer's disease has now been supported by a finding that in genetically engineered mice, loss of smell function is associated with amyloid-beta accumulation in the brain, and that amyloid pathology occurs first in the olfactory region. It was striking how sensitive olfactory performance was to even the smallest amount of amyloid presence in the brain as early as three months of age (equivalent to a young adult).
Mental fluctuations may signal Alzheimer's disease
A study involving 511 older adults (average age 78) has found that 11.6% of those with very mild or mild Alzheimer’s (43% of the participants) had mental lapses, compared to only 2 of the 295 without Alzheimer’s. Those with mental lapses also tended to have more severe Alzheimer’s. Although mental lapses are characteristic of dementia with Lewy bodies, this is the first study to look at them in connection with Alzheimer’s. Having mental lapses was defined as having three or four of the following symptoms:
Higher levels of copper in amyloid plaques associated with degree of neurodegeneration
Following on from the evidence that Alzheimer’s brains show higher levels of metals such as iron, copper, and zinc, a mouse study has found that amyloid plaques in Alzheimer’s-like brains with significant neurodegeneration have about 25% more copper than those with little neurodegeneration. This is consistent with a human study showing very high levels of copper in Alzheimer’s plaques.
Iron, though doubled in Alzheimer’s brains compared to controls, was not significantly different as a function of neurodegeneration, and zinc showed very little difference.
Plaques tell which MCI patients will progress to Alzheimer’s
A three-year study involving 152 adults aged 50 and older, of whom 52 had been recently diagnosed with mild cognitive impairment and 31 were diagnosed with Alzheimer's disease, has found that those with mild or no cognitive impairment who initially had amyloid-beta plaques showed greater cognitive decline than those whose brain scans were negative for plaques. Moreover, 35% of plaque-positive participants who started with MCI progressed to Alzheimer's, compared to 10% without plaque, and they were more than twice as likely to be started on cognitive-enhancing medication.
Tracking preclinical Alzheimer's progression
New research supports the classification system for preclinical Alzheimer’s proposed two years ago. The classification system divides preclinical Alzheimer's into three stages:
Stage 1: Levels of amyloid beta begin to decrease in the spinal fluid. This indicates that the substance is beginning to form plaques in the brain.
Stage 2: Levels of tau protein start to increase in the spinal fluid, indicating that brain cells are beginning to die. Amyloid beta levels are still abnormal and may continue to fall.
New biomarker shows Alzheimer's disease long before symptoms
Analysis of mitochondrial DNA (mtDNA) in the cerebrospinal fluid has found that both symptomatic Alzheimer’s patients and asymptomatic patients at risk of Alzheimer’s showed a significant decrease in levels of circulating cell-free mtDNA in the CSF. Patients with frontotemporal dementia did not display this.
One Alzheimer's risk gene may begin to affect brains from childhood
A gene linked to Alzheimer's has been linked to brain changes in childhood. This gene, SORL1, has two connections to Alzheimer’s: it carries the code for the sortilin-like receptor, which is involved in recycling some molecules before they develop into amyloid-beta; it is also involved in lipid metabolism, putting it at the heart of the vascular risk pathway.
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