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Proceedings of the National Academy of Sciences of the United States of America,


**15** 

**Tau and Amyloid-β Conformational Change** 

Martha A. De Anda-Hernández1\*, Karla I. Lira-De León1\*, Raúl Mena2,

*3Experimental Laboratory of Neurodegenerative Diseases, Neurology and Neurosurgery* 

The pathology of Alzheimer Disease (AD) has been intensely studied in the last 20 years (Duyckaerts et al., 2009) because it is a progressive neurodegenerative disorder that causes dementia in approximately 10% of individuals older than 65 years (Hampel et al., 2010). AD occurs gradually; starting with the so called mild cognitive impairment (MCI) recognized by mild memory disturbances and noticed difficulties in performing more demanding cognitive tasks. With disease progression the decline in memory and cognition become more expressed and are accompanied by changes in personality and behaviour. In later stages of the disease loss of speech and movement is followed by total disability and finally death. A person with AD lives on average eight years after the onset of symptoms (Zerovnik, 2010). Actual studies are focused in many strategies for markers of susceptibility, early diagnostic, understanding of molecular mechanism, effective treatment and preventing strategies. According to Duyckaerts and coworkers (2009) AD could be divided in three broad chapters: lesions related to abnormal accumulation of proteins, those that are due to neural losses and finally those that are due to the reactive processes. According to abnormal accumulations proteins, AD is characterized by the presence of two types of neuropathological hallmarks: neurofibrillary tangles (NFTs) and neuritic plaques (NP). NFTs are intraneuronal aggregates of abnormally modified Tau (phosphorylated at non physiological sites, truncation, etc). NP are extracellular and mainly composed of amyloid βpeptide (AB) deposits (Martin et al., 2011). The most of the cases of AD are reported as "sporadic" pathway, because we still do not know what could be the factors that lead to this disease. Many hypotheses has been proposed, including immune system participation (Solomon &Frenkel, 2010), pathogens (Miklossy, 2011), oxidative stress responses, and more. At the end, in patients we can always find NFTs and NP in several regions of the brain

**1. Introduction** 

 \*

Both authors contributed in the same manner

 **to β-Sheet Structures as Effectors in the** 

*2Physiology, Biophysics and Neurosciences Department, CINVESTAV-IPN,* 

**Development of Alzheimer's Disease** 

Victoria Campos-Peña3 and Marco A. Meraz-Ríos1 *Center of Research and Advanced Studies, CINVESTAV-IPN, 1Molecular Biomedicine Department, CINVESTAV-IPN,* 

*National Institute (INNN),* 

*Mexico* 

