01.01.2014, Impact of Vitamin D on Amyloid Precursor Protein Processing and Amyloid-β Peptide Degradation in Alzheimer's Disease

Neurodegener Dis. 2014;13(2-3):75-81.


Grimm MO, Lehmann J, Mett J, Zimmer VC, Grösgen S, Stahlmann CP, Hundsdörfer B, Haupenthal VJ, Rothhaar TL, Herr C, Bals R, Grimm HS, Hartmann T

Several studies indicate a link between Vitamin D and Alzheimer’s disease. However, the underlying mechanism is not understood. Vitamin D hypovitaminosis affects up to 90% of the elderly population and has been reported to be associated with decreased cognitive function. Here we have examined the underlying mechanism, showing that both, Ab production and degradation, is affected already by a mild to moderate Vitamin D hypovitaminosis in mice and cell culture, leading to a changed Ab level. The enzymes involved in this processes are identified to be b-secretase and neprilysin.

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01.01.2014, Hippocampus-related cognitive impairments in young apoE4 targeted replacement mice.

Neurodegener Dis. 2014; 13(2-3):86-92.


Salomon-Zimri S, Boehm-Cagan A, Liraz O, Michaelson DM.

ApoE4 is the major genetic risk factor for Alzheimer's disease. We have previously shown that the pathological effects of apoE4 can be detected in young, naïve apoE4 targeted replacement mice. This study shows that the apoE4 mice show distinct cognitive deficits in a variety of hippocampus related behavioral paradigms. These behavioral paradigms can be utilized to assess the effectiveness of novel treatments.

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01.01.2014, Targeting synaptic dysfunction in Alzheimer’s disease by administering a specific nutrient combination

J Alzheimers Dis. 2014; 38(3):459-79.


Nick van Wijk, Laus M. Broersen, Martijn C. de Wilde, Robert J.J. Hageman, Martine Groenendijk, John W.C. Sijben, and Patrick J.G.H. Kamphuis

A loss of synaptic connections in the brain is believed to occur already in the early stages of Alzheimer’s disease. A specific combination of nutrients necessary for the formation of new synaptic connections has been designed that may fulfill the specific nutritional needs of Alzheimer patients. In this publication the LipiDiDiet researchers review the available scientific evidence on how these nutrients act together to induce beneficial effect in various experimental models.

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01.01.2014, Midlife and late-life body mass index and late-life dementia: results from a prospective population-based cohort

Journal of Alzheimer’s Disease, 2014; 38(1):201-209


Tolppanen AM, Ngandu T, Kåreholt I, Laatikainen T, Rusanen M, Soininen H, Kivipelto M.

The aim of this study was to investigate the association of midlife and late-life body mass index (BMI) with late-life dementia/Alzheimer's disease (AD) and whether the association was independent of other obesity-related co-morbidities. Higher midlife BMI was related to higher risk of dementia and AD, independently of obesity-related risk factors and co-morbidities. Steeper decrease of BMI and low late-life BMI were associated with higher risk of dementia and AD. These findings highlight the importance of life-course perspective when assessing the association between BMI and cognition.

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23.12.2013, Neprilysin and Aβ Clearance: Impact of the APP Intracellular Domain in NEP Regulation and Implications in Alzheimer's Disease.

Front Aging Neurosci. 2013 Dec 23;5:98.


Grimm MO, Mett J, Stahlmann CP, Haupenthal VJ, Zimmer VC, Hartmann T.

One of the charateristic pathological hallmarks of Alzheimer´s diesease is the accumulation of Amyloid b (Ab). The level of Amyloid b is not only affected by the rate of the de novo synthesis but also by its degradation. One of the major enzymes of the Ab degradation is Neprilysin. In this overview article we summarize the most important facts about the regulation of NEP and its implication in Alzheimer´s disease.

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