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The presubiculum is preserved from neurodegenerative changes in Alzheimer's disease

Artikel i vetenskaplig tidskrift
Författare C. E. Murray
P. Gami-Patel
Eleni Gkanatsiou
Gunnar Brinkmalm
Erik Portelius
O. Wirths
W. Heywood
Kaj Blennow
J. Ghiso
J. L. Holton
K. Mills
Henrik Zetterberg
T. Revesz
T. Lashley
Publicerad i Acta Neuropathologica Communications
Volym 6
Nummer/häfte 62
ISSN 2051-5960
Publiceringsår 2018
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
Språk en
Länkar dx.doi.org/10.1186/s40478-018-0563-...
Ämnesord Alzheimer's disease, Presubiculum, Amyloid, Tau, Neuroinflammation, familial british dementia, amyloid beta-peptides, a-beta, precursor, protein, human brain, mouse model, in-vivo, parvopyramidal layer, danish, dementia, senile plaques, Neurosciences & Neurology, iences
Ämneskategorier Neurokemi

Sammanfattning

In the majority of affected brain regions the pathological hallmarks of Alzheimer's disease (AD) are beta-amyloid (A beta) deposits in the form of diffuse and neuritic plaques, tau pathology in the form of neurofibrillary tangles, neuropil threads and plaque-associated abnormal neurites in combination with an inflammatory response. However, the anatomical area of the presubiculum, is characterised by the presence of a single large evenly distributed 'lake-like' A beta deposit with minimal tau deposition or accumulation of inflammatory markers. Post-mortem brain samples from sporadic AD (SAD) and familial AD (FAD) and two hereditary cerebral amyloid diseases, familial British dementia (FBD) and familial Danish dementia (FDD) were used to compare the morphology of the extracellular proteins deposited in the presubiculum compared to the entorhinal cortex. The level of tau pathology and the extent of microglial activation were quantitated in the two brain regions in SAD and FAD. Frozen tissue was used to investigate the A beta species and proteomic differences between the two regions. Consistent with our previous investigations of FBD and FDD cases we were able to establish that the 'lake-like' pre-amyloid deposits of the presubiculum were not a unique feature of AD but they also found two non-A beta amyloidosis. Comparing the presubiculum to the entorhinal cortex the number of neurofibrillary tangles and tau load were significantly reduced; there was a reduction in microglial activation; there were differences in the A beta profiles and the investigation of the whole proteome showed significant changes in different protein pathways. In summary, understanding why the presubiculum has a different morphological appearance, biochemical and proteomic makeup compared to surrounding brain regions severely affected by neurodegeneration could lead us to understanding protective mechanisms in neurodegenerative diseases.

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