Neural Regeneration Research ›› 2023, Vol. 18 ›› Issue (1): 119-120.doi: 10.4103/1673-5374.340403

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Misfolded amyloid-β strains and their potential roles in the clinical and pathological variability of Alzheimer’s disease

Sara Kelley, Nelson Perez-Urrutia, Rodrigo Morales*   

  1. Department of Neurology, University of Texas Health Science Center at Houston, Houston, TX, USA (Kelley S, Perez-Urrutia N, Morales R)
    Centro Integrativo de Biologia y Quimica Aplicada (CIBQA), Universidad Bernardo O’Higgins, Santiago, Chile (Morales R)

  • Online:2023-01-15 Published:2022-06-17
  • Contact: Rodrigo Morales, PhD, Rodrigo.MoralesLoyola@uth.tmc.edu.
  • Supported by:
    This work was supported by grants from the Alzheimer’s Association (AARGD-18-566576), NIH/NIA (RF1AG072491) and NIH/NIAID (R01AI132695) to RM. 

Abstract: Potential causes for the clinical and pathological variability observed in Alzheimer’s disease (AD): AD is an age-related neurodegenerative disorder characterized by the impairment of cognitive functions such as memory, learning, and reasoning. These commonly described clinical symptoms are due to particular pathological changes in the brain, including inflammation, synaptic loss, and neuronal death. These changes are a consequence of the accumulation of abnormally folded amyloid-β (Aβ) and tau proteins in specific areas of the central nervous system. Considering the progressive aging of the world’s population, the number of people affected by AD is expected to substantially and consistently increase in the coming years. This positions AD as one of the main public health challenges in the near future.