Intraneuronal Aβ: Was It APP All Along?
secrete Aβ has stood the test of time and drawn the field’s main focus firmly to the outside of neurons
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secrete Aβ has stood the test of time and drawn the field’s main focus firmly to the outside of neurons
On 19 April 2011, the National Institute on Aging (NIA) and the Alzheimer’s Association (AA)
more amyloid-β peptide in their brains than normal and, in time, they all develop Alzheimer
Alzheimer’s disease. There, microglia cluster around amyloid-β plaques (Naert and Rivest, 2011). One and the
Jersey, believes that the time has come to reassess what we know about AD, focusing less on amyloid and
work on herpes simplex virus type 1 (HSV1) and Brian Balin ’s data showing induction of amyloid plaques
sclerosis and frontotemporal lobar degeneration, where stress granule markers decorate pathological protein
hippocampus and cortex have grabbed the lion’s share of attention in Alzheimer’s disease, leaving other brain
the clinical dementia rating scale and against neuropsychological tests, and is available in several
most of the Americas, parts of Europe, and Asia. For Alzheimer disease, amyloid imaging with PET
in its own way.” The same might be said of the brain. Normal brains look and behave similarly, but
background in AD biomarker studies, or for those who simply had no time to absorb the 10-page article and its
for the discussion were Pierre Tariot (Banner Alzheimer's Institute), John Ringman (UCLA), and
Carrillo, who directs medical and scientific relations at the Alzheimer’s Association, a funding
patients in the context of drug discovery with special emphasis on Alzheimer disease and schizophrenia,
Have a topic idea for a webinar? We would love to hear it. Send an email to webinars [at] alzforum [dot] org.