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. 2019 Jun;34(6):781-789.
doi: 10.1002/gps.5088. Epub 2019 Mar 15.

Delirium and Alzheimer disease: A proposed model for shared pathophysiology

Tamara G Fong  1   2   3 , Sarinnapha M Vasunilashorn  3   4 , Towia Libermann  3   5   6 , Edward R Marcantonio  3   4 , Sharon K Inouye  2   3   4
Affiliations

Delirium and Alzheimer disease: A proposed model for shared pathophysiology

Tamara G Fong et al. Int J Geriatr Psychiatry. 2019 Jun.
No abstract available

Keywords: biomarkers; delirium; dementia.

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Figures

Figure 1.
Figure 1.. Conceptual model for the interrelationship between delirium and AD.
Grey boxes indicate the baseline brain status (far left panel, BASELINE) delirium “state” (middle panels, ACUTE and CONVALESCENT), or outcome (far right panel, OUTCOME); white boxes indicate corresponding (hypothesized) biomarker level. Solid arrows indicate hypothesized pathways for development of delirium (gray),complicated delirium (black), or no delirium (white); dashed arrows indicate where exceptions can occur. 1This figure is intended to represent the most likely pathways for outcomes but there are exceptions. For example, a patient with a resilient brain (upper box, far left panel) could develop a severe delirium, if the delirium trigger was sufficiently noxious (lower box, second panel from left) and ultimately develop long-term cognitive decline or ADRD; likewise someone with a vulnerable brain (lower box, far left) who is resilient to the delirium trigger because of high cognitive reserve might develop a mild delirium (middle box, second panel from left) and go on to recover (upper box, far right panel) 1 Delirium can be triggered by a range of insultsincluding surgery, infections, hypoxia, metabolic abnormalities, stroke, drugs, or anesthetics, and these insults can vary in severity and duration 2 Abnormal risk biomarkers (at baseline) of a vulnerable brain might reflect inflammation, oxidative stress, or chronic neurodegeneration present at basal level 3 Abnormal biomarkers triggered by delirium mightreflect inflammation, alterations in neurotransmitter function, neuronal or microglial dysfunction, or neuronal death, or acceleration of underlying chronic processes. As biomarkers become increasingly abnormal, deliriumseverity may increase as well. 4 Abnormal end product (i.e., neuronal injury/cell death) biomarkers emerge in the convalescent phase when disease processes are sufficient during the acute phase to trigger neuronal injury. Note: This model will accommodate multiple putative biomarkers. For example, anemia can still be integrated into our conceptual model, as a risk or disease marker that is contributory along the pathway to neuronal injury. abbreviations: AD=Alzheimer’s disease; ADRD=Alzheimer’s disease and relateddementias; LTCD=long-term cognitive decline; MCI=mild cognitive impairment
See this image and copyright information in PMC

References

    1. Oh ES, Fong TG, Hshieh TT, Inouye SK. Delirium in Older Persons: Advances in Diagnosis and Treatment. JAMA. 2017;318(12):1161–1174. - PMC - PubMed
    1. Fick DM, Agostini JV, Inouye SK. Delirium superimposed on dementia: a systematic review. J Am Geriatr Soc. 2002;50(10):1723–1732. - PubMed
    1. Oh ES, Fong TG, Hshieh TT, Inouye SK. Delirium in Older Persons: Advances in Diagnosis and Treatment. JAMA. 2017;318(12):1161–1174. - PMC - PubMed
    1. Fong TG, Davis D, Growdon ME, Albuquerque A, Inouye SK. The interface between delirium and dementia in elderly adults. Lancet Neurol. 2015;14(8):823–832. - PMC - PubMed
    1. Hshieh TT, Fong TG, Marcantonio ER, Inouye SK. Cholinergic deficiency hypothesis in delirium: a synthesis of current evidence. J Gerontol A Biol Sci Med Sci. 2008;63(7):764–772. - PMC - PubMed