Stuck in the Past? Microglial Memories Dictate Response to Aβ
Systemic inflammation can alter the epigenome of microglia, dictating whether the cells clean up Aβ pathology, or exacerbate it.
NEWS
Genetics Tie ALS into the Frontotemporal Dementia Spectrum
Massive meta-analysis finds no link with AD or PD.
Does Amyloid Accumulate After a Single Sleepless Night?
Volunteers kept awake all night retained more florbetaben in their hippocampi and thalami in morning-after PET scan.
Do Immune Responses Promote, or Prevent, Parkinson’s Disease?
In animal models, a PD risk gene revs up the immune system to fight infections, while probiotic bacteria slow α-synuclein aggregation.
Parkinson’s Treatments Go After Genetic Targets
Researchers at AAT-AD/PD discussed investigational PD treatments that aim to modify disease by hitting genetic risk factors.
New Definition of Alzheimer’s Hinges on Biology, Not Symptoms
For the first time, NIA-AA proposal bases diagnosis in living people solely on biomarkers for plaques and tangles.
Is Shape of Aβ an Early Blood Biomarker for Alzheimer’s?
An infrared spectral signature of amyloid β-sheets predicted AD conversion years before diagnosis.
Newborn Neurons in the Adult Brain: Real Deal, or Glial Imposters?
A study reported that new neurons continue to sprout from the human hippocampus well into the golden years, while another claims they all but disappear after childhood.
SPOTLIGHT
Microglial Memories May Sway Responses to Aβ
Bouts of systemic inflammation have long-lasting effects on microglia in the brain, according to a new study. Researchers reported that depending on how many times mice were injected with bacterial lipopolysaccharides, microglia either slowed the growth of Aβ plaques, or accelerated it. Exposure to systemic inflammation, and/or to Aβ pathology within the brain, influenced the epigenomes of microglia, in turn altering their gene-expression profiles and function.
Biology Ascendant: Alzheimer’s Defined Sans Symptoms
Toppling the long-standing syndromic definition of AD, scientists now embrace a biologically based concept to diagnose Alzheimer’s disease in living people. Using biochemical tests and scans to detect pathologic protein accumulation, they separate the diagnosis from symptoms. The proposal marks a seismic shift away from distinct, clinically defined entities and toward a continuous disease process defined by its underlying pathophysiology. It is for research use only.
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