Analysis of 40 spinal marrow samples, 20 of which belonged to Alzheimer’s patients, has identified six proteins in spinal fluid that can be used as markers for Alzheimer's. The analysis focused on 35 proteins that are associated with the lysosomal network — involved in cleaning and recycling beta amyloid.
Data from 848 adults of all ages has found that brain volume in the default mode network declined in both healthy and pathological aging, but the greatest decline occurred in Alzheimer’s patients and in those who progressed from mild cognitive impairment to Alzheimer’s disease.
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.
Initial findings from an analysis of cerebrospinal fluid taken between 1995 and 2005 from 265 middle-aged healthy volunteers, of whom 75% had a close family member with Alzheimer’s disease, has found that the ratios of phosphorylated tau and amyloid-beta could predict mild cognitive impairment more than five years before symptom onset — the more tau and less amyloid-beta, the more likely
People with Parkinson’s disease have a six times greater risk of developing dementia than the general population. A new study points to a way of picking out those who are at risk of dementia.
A five-year study involving 525 older adults (70+) found 46 had Alzheimer’s or aMCI and a further 28 went on to develop the conditions. The blood levels of 10 specific lipids predicted with more than 90% accuracy whether an individual would go on to develop either Alzheimer’s or aMCI within 2-3 years. The researchers speculate that the lower lipid levels could be an early indication that brain cells are beginning to lose their integrity and break down.
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.
More evidence for early changes in the eye in Alzheimer’s disease comes from a study involving both rats and postmortem human retinas. Changes were found in the retinal pigment epithelial layer (which harbors the supportive cells located in the back of the eye) and in the thickness of the choroidal layer that has blood vessels providing nutrients to the retina.
The finding is consistent with growing evidence that glaucoma is a neurodegenerative disorder similar to Alzheimer’s.
A multi-year study involving 207 healthy older adults, in which their spinal fluids were repeatedly sampled and their brains repeatedly scanned, has found that disruptions in the default mode network emerges about the same time as chemical markers of Alzheimer’s appear in the spinal fluid (decreased amyloid-beta and increased tau protein). The finding suggests not only that amyloid-beta and tau pathology affect default mode network integrity early on, but that scans of brain networks may be an equally effective and less invasive way to detect early disease.
An analysis of the anatomical connectivity in the brains of 15 people with Alzheimer's disease, 68 with mild cognitive impairment and 28 healthy older individuals, has found several measures showed disease effects: