Amyloid pathology and synaptic loss in pathological aging

Abstract

This is an open access article under the terms of the Creat ive Commo ns Attri bution-NonCo mmercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

Aging, Neurodegenerative Disorders, and Cerebellum

“…Such reduction in the receptor expression might adversely affect cerebellar Ca 2+ signaling and synaptic function [53]. Interestingly, the cerebellum of patients with AD demonstrated no visible pathological changes, only moderate alterations in the levels of synaptic proteins, few amyloid plaques, and a relatively equal amount of the Aβ isoforms Aβ40 and Aβ42 [54]. Similarly, aged female Lewis rats demonstrated no age-dependent changes in citrate synthase (CS) activity or the protein levels or enzymatic activity of mitochondrial complexes I-V, all of which serve as markers of mitochondrial biogenesis, mitophagy, fusion, and fission of cerebellum [55].…”

Preface: Mass spectrometry in Alzheimer disease

“…They survey how specifically in situ and ex situ techniques are used together with MS techniques to characterize pathogenic Aβ-and Tau species, such as oligomers, associated with the pathogenic processes underlying AD. Following this introduction, Tammaryn Lashley and colleagues from the UCL Queen Square Brain Bank demonstrate in their contribution how those bottom-up strategies reviewed above can be employed to comprehensively interrogate Aβ profiles across heterogenic plaque pathology in post mortem brain tissue from both AD-as well as cognitively unimpaired individuals (Gkanatsiou et al, 2021). Staying within the realm of in situ mass spectrometry analysis of AD pathology, Schrader et al present data on protein features associated with cerebral amyloid angiopathy (CAA) deposition in a rat model of vascular amyloid pathology (Schrader et al, 2021).…”