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P2‐258: AMYLOID DEPOSITS IMAGED IN POSTMORTEM RETINAS USING POLARIMETRY PREDICT THE SEVERITY OF A POSTMORTEM BRAIN BASED DIAGNOSIS OF ALZHEIMER'S DISEASE
Author(s) -
Campbell Melanie C.W.,
Emptage Laura,
Redekop Rachel,
Corapi Frank,
Mason Erik,
Hirsch-Reinshagen Veronica,
Kitor Monika,
Shah Namrata,
Hamel Michael T.,
Robin Hsiung Ging-Yuek,
Mackenzie Ian R.
Publication year - 2018
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2018.06.947
Subject(s) - retina , pathology , retinal , senile plaques , amyloid (mycology) , alzheimer's disease , medicine , biology , ophthalmology , disease , neuroscience
(SCFA). The search yielded human cell culture experiments and clinical trial publications. Results: There is evidence that the gutbrain axis is influenced by the dysbiosis-provoked inflammation. Similar bacterial dysbiosis was found in both T2D and AD. A strong correlation between high levels of pro-inflammatory bacteria and CSF p-tau/Aß42 has been documented. To further the process of AD pathology, insulin degrading enzyme (IDE) secretion via the autophagy-lysosome pathway are reduced by the increased levels of tau-p and Aß levels, which have been associated with direct breakdown of the autophago-lysosomal pathway. Additionally, there is a negative association between a reduced anti-inflammatory bacterial load and AD pathology. These bacteria produce SCFA, which have powerful anti-inflammatory effects. SCFA inhibit the NF-kB/miRNA125 pathway, thereby promoting neuroprotection. There is less clinical evidence for the influence of the cerebral IR in AD. However, one of the studies using PIB-PET scan measured excess amyloid deposition in those suffering from cerebral IR despite participants being normoglycemic. Conclusions: Gut dysbiosis can lead to insulin resistance in T2D and AD through inflammatory mechanisms. There is evidence that cerebral IR enhance the early underlying pathological events in AD. Moreover, pre-diabetic and diabetic states further exacerbate pathological processes implicated in AD, with some evidence pointing to the promotion of cerebral IR in the presence of peripheral IR.