Good news! Getting the details right may make a huge difference!
"... The international research team that analyzed cerebrospinal fluid proteins in 606 people says this means that medications already tested may have falsely seemed to be ineffective or only slightly effective.
Their discovery could lead to more personalized therapies or preventive measures for these subtypes. It also presents hope for early diagnosis and intervention to delay the onset of symptoms of Alzheimer's disease (AD). ...
The researchers were able to identify five distinct biological subtypes of the disease, distinguished by variations such as hyperplasticity, immune activation, RNA dysregulation, choroid plexus dysfunction, and blood-brain barrier impairment. ..."
From the abstract:
"Alzheimer’s disease (AD) is heterogenous at the molecular level. Understanding this heterogeneity is critical for AD drug development. Here we define AD molecular subtypes using mass spectrometry proteomics in cerebrospinal fluid, based on 1,058 proteins, with different levels in individuals with AD (n = 419) compared to controls (n = 187). These AD subtypes had alterations in protein levels that were associated with distinct molecular processes: subtype 1 was characterized by proteins related to neuronal hyperplasticity; subtype 2 by innate immune activation; subtype 3 by RNA dysregulation; subtype 4 by choroid plexus dysfunction; and subtype 5 by blood–brain barrier impairment. Each subtype was related to specific AD genetic risk variants, for example, subtype 1 was enriched with TREM2 R47H. Subtypes also differed in clinical outcomes, survival times and anatomical patterns of brain atrophy. These results indicate molecular heterogeneity in AD and highlight the need for personalized medicine."
Fig. 1: Biological description of AD subtypes.
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