Abstract
Alzheimer’s Disease (AD) is the most common form of dementia [1]. Patients diagnosed with AD experience disordered cognition and memory, as well as changes in behaviour and personality [2]. The vast majority of AD is diagnosed in patients aged over 65 years and classified as late onset (LOAD), with the remaining ~1% of cases termed early onset AD (EOAD) [3]. The molecular neuropathology of AD includes the presence of extracellular amyloid beta (Ab)
plaques and proteinaceous lesions of aggregated neuronal tau protein across multiple brain regions [4,5]. Implicated regions include brainstem structures as the origin of progressive neurodegeneration [6,7], which then follows a predictable spreading pattern to the cholinergic basal forebrain [8], the (trans)entorhinal cortex, hippocampus, and the neocortex [9].
plaques and proteinaceous lesions of aggregated neuronal tau protein across multiple brain regions [4,5]. Implicated regions include brainstem structures as the origin of progressive neurodegeneration [6,7], which then follows a predictable spreading pattern to the cholinergic basal forebrain [8], the (trans)entorhinal cortex, hippocampus, and the neocortex [9].
Original language | English |
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Pages (from-to) | 78-81 |
Number of pages | 4 |
Journal | Journal of Experimental Neurology |
Volume | 3 |
Issue number | 3 |
DOIs | |
Publication status | Published - 2022 |
Keywords
- neuropathology
- Alzheimer's Disease
- Tau protein
- Amyloid beta