Alzheimers disease and epilepsy are reciprocally related. Among sporadic AD patients, seizures occur in 10-22 percent, and subclinical epileptiform abnormalities occur in 22-5 percent. Cognitive deficits, with prominent short-term memory impairments, occur in most epilepsy patients. Common neurophysiological and molecular mechanisms occur in AD and epilepsy. Emerging evidence identifies choroid plexus pathological changes in aging, AD, and epilepsy. These include decreased CSF turnover, A-beta and tau accumulation with impaired clearance, and disrupted CSF amino acid homeostasis; this pathology may contribute to synaptic dysfunction in AD and epilepsy.
We found altered signaling pathways in the choroid plexus of severe AD cases and many correlated changes in protein expression of cell metabolism pathways in AD and epilepsy cases. Shared molecular mechanisms should be investigated further to distinguish pathogenic from secondary changes. This could inform novel therapeutic strategies to prevent disease progression or restore normal function. Focusing on dual-diagnosed AD/epilepsy cases, specific epilepsy syndromes like temporal lobe epilepsy, and changes across different severity levels in AD and epilepsy would significantly add to our understanding.
[doi:10.25345/C5HM52V66]
[dataset license: CC0 1.0 Universal (CC0 1.0)]
Keywords: FFPE ; AD ; epilepsy ; LFQ ; proteomics ; DIA
Principal Investigators: (in alphabetical order) |
Beatrix Ueberheide, NYU School of Medicine, USA |
Submitting User: | KanshinED1 |
Leitner DF, Kanshin E, Faustin A, Thierry M, Friedman D, Devore S, Ueberheide B, Devinsky O, Wisniewski T.
Localized proteomic differences in the choroid plexus of Alzheimer's disease and epilepsy patients.
Front Neurol. Epub 2023 Jul 14.
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