The study of golgi apparatus in alzheimer's disease

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Neurochem Res (2007) 32:1265–1277 DOI 10.1007/s11064-007-9302-4


The Study of Golgi Apparatus in Alzheimer’s Disease
Zhiping Hu Æ Liuwang Zeng Æ Zhiling Huang Æ Jie Zhang Æ Ting Li

Accepted: 30 January 2007 / Published online: 31 March 2007 Ó Springer Science+Business Media, LLC 2007

Abstract Alzheimer’s disease is an irreversible, progressive neurodegenerative disorderleading invariably to death, usually within 7–10 years after diagnosis and is the leading cause of dementia in the elderly. Not only is Alzheimer’s disease a tragic disease in which people suffer from neurodegeneration in the years to come, it also becomes an incredible burden on the public health system. However, there is currently no effective treatment to halt the progression or prevent the onset ofAlzheimer’s disease. This is partly due to the fact that the complex pathophysiology of Alzheimer’s disease is not yet completely understood. Recently, Golgi apparatus is found to play an important role in Alzheimer’s disease. In this review, we discuss the changes of Golgi apparatus during clinical progression and pathological development of Alzheimer’s disease. First, changes of Golgi apparatussize in Alzheimer’s disease are summarized. We then address the role of Golgi apparatus in the neuropathology of Alzheimer’s disease. Finally, the role of Golgi apparatus in the pathogenesis of Alzheimer’s disease is discussed. Understanding the contribution of Golgi apparatus dysfunction to Alzheimer’s disease and its pathophysiological basis will significantly impact our ability to develop moreeffective therapies for Alzheimer’s disease. Keywords Golgi apparatus Á Alzheimer’s disease Á Amyloid b-protein Á Amyloid precursor protein Á Presenilins Á Gamma-secretase Á Tau

Abbreviations Ab amyloid b-protein AD Alzheimer’s disease APP amyloid-beta precursor protein BACE beta-site APP-cleaving enzyme CTFs C-terminal fragments ER endoplasmic reticulum ERGIC ER-Golgi intermediate compartmentFAD familial Alzheimer’s disease GA Golgi apparatus iAbeta intracellular Abeta MCI mild cognitive impairment MMN the medial mamillary nucleus NBM nucleus basalis of Meynert NCI no cognitive impairment NFTs neurofibrillary tangles PM plasma membrane PHFs paired helical filaments PS Presenilin SorLA Sorting protein-related receptor SPs ‘‘senile’’ plaques TGN trans-Golgi network TMN tuberomamillarynucleus VDB the vertical limb of the diagonal band of Broca

Z. Hu Á L. Zeng (&) Á Z. Huang Á J. Zhang Á T. Li Department of Neurology, Second Xiangya Hospital, Central South University, Changsha 410011, China e-mail:

Alzheimer’s disease (AD) was first described by Alois Alzheimer in 1907.It is a late-onset and progressive neurodegenerative disordercharacterized clinically by memory loss, impairment of other cognitive functions,



Neurochem Res (2007) 32:1265–1277

and changes in behavior and personality. The current estimate for people suffering from Alzheimer’s disease is close to 15–20 million people worldwide [1]. Approximately 1% of people aged 65–69, 3% aged 70– 74, 6% aged 75–79, 12% aged 80–84 and 25% aged 85 and over willdevelop Alzheimer’s disease [2]. As the population grows and average life spans continue to lengthen, the prevalence of Alzheimer’s disease is predicted to be between 30 and 40 million worldwide by 2050 [1]. The ‘‘senile’’ plaques (SPs) and neurofibrillary tangles(NFTs) are the two characteristic pathological features of Alzheimer’s disease. Whereas tangles consist of the peptide tau, neuriticplaques primarily consist of deposits of amyloid b (Ab), a 39–43 amino acid peptide that is derived through the processing of amyloid precursor protein.The etiology of Alzheimer’s disease is unclear.In familial Alzheimer’s disease, mutations in the gene encoding the amyloid precursor protein (APP) and presenilins 1 and 2 (PS1 and PS2) have been linked to development of Alzheimer’s disease in humans....
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