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Updated: Aug 14, 2026

Quantitative 3D In Silico Modeling (q3DISM) of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
Published on: December 26, 2016
[Systemic changes of the immune system in patients with Alzheimer's dementia]
F Leblhuber1, J Walli, G P Tilz
1Abteilung für Neurologisch-Psychiatrische Gerontologie, Landesnervenklinik Wagner-Jauregg, Linz.
Objective:
The etiology of Alzheimer's disease (AD) is still unknown. Recent investigations have shown that immune and inflammatory mechanisms could be of importance in the pathophysiology of AD. In this study 10 different immune parameters were measured to further investigate immunological changes in AD.
Patients And Methods:
In 30 randomized patients with AD (20 females and ten males aged 74.5 +/- 6.5 years) as well as 13 controls aged 70.7 +/- 8.4 years, mostly relatives of the patients, all free of acute infection, serum concentrations of IgA, IgG, IgM, C3, C4, circulating immune complexes, sCD23, cardiolipin and the soluble cytokine receptors interleukin 2-receptor (sIL2-R) and tumor necrosis factor-receptor (sTNF-R) were measured. Diagnosis of AD was made according to NINCDS/ ADRDA criteria. The degree of dementia was determined by Mini-Mental-State-Examination (MMSE).
Results:
Compared to the control group, patients with AD had significantly increased IgA (369,3 +/- 160,9 mg/dl vs 253.5 +/- 101.8 mg/dl [P = 0.02]), sCD23 [207.4 +/- 217.7 I. U./ml vs 80.6 +/- 35.5 I. U./ml [P = 0.004]), sIL2-R (829.6 +/- 742.1 I. U./ml vs 299.7 +/- 168.5 I. U./ml [P = 0.001]) and sTNF-R (4.6 +/- 2.0 I. U./ml vs 2.9 +/- 1.1 I. U./ml [P = 0.001]) levels. A negative correlation was seen between MMSE and sTNF-R (r = -0.34; P < 0.05).
Conclusion:
These findings indicate a chronic state of immune activation in AD and support the hypothesis of immune mediated mechanisms as part of the pathogenesis of AD. Prospective studies of the effect of anti-inflammatory drugs on the progression of AD will be needed.
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