Álvarez SM, Pedroso I, de la Fe A, Padrón SA, Álvarez SM, Álvarez L

Language: Spanish
References: 20
Page: 196-201
PDF size: 93.82 Kb.

ABSTRACT

Alzheimer disease is the most common cause of dementia. Its pathological land marks are the extracelular accumulation of amyloid plaques and the intracellular neurofibrilar tangles. In this paper we review the pathophysiology at anatomical, molecular and genetics levels and analyze the importance for developing symptoms. These concepts are the base for future treatments.

REFERENCES

1. Khachaturian ZS. Diagnosis of Alzheimer Disease. Arch Neurol 1985; 42: 1097-105.

2. Engler H, Forsberg A, Almkvist O, Blomquist G, Larsson E, Savitcheva I, et al. Two-year follow-up of amyloid deposition in patients with Alzheimer’s disease. Brain 2006; 129(Pt. 11): 2856-66.

3. Wang L, Zhu M, Li X, Gui Q. [The application of Gallyas-Braak stainings in pathologic diagnosis of neurodegenerative diseases]. Zhonghua Nei Ke Za Zhi 2002; 41(2): 120-3.

4. Masters CL, Simms G, Weinman NA, Multhaup G, McDonald BL, Beyreuther K. Amyloid plaque core protein in Alzheimer disease and Down syndrome. Proc Natl Acad Sci USA 1985; 82: 4245-49.

5. Gandy S. The role of cerebral amyloid beta accumulation in common forms of Alzheimer disease. J Clin Invest 2005; 115: 1121-29.

6. Carson JA, Turner AJ. Beta-amyloid catabolism: roles for neprilysin (NEP) and other metallopeptidases? J Neurochem 2002; 81: 1-8.

7. Tanzi RE, Moir RD, Wagner SL. Clearance of Alzheimer’s Abeta peptide: the many roads to perdition. Neuron 2004; 43: 605-08.

8. Grundke-Iqbal I, Iqbal K, Tung YC, Quinlan M, Wisniewski HM, Binder LI. Abnormal phosphorylation of the microtubule-associated protein τ (tau) in Alzheimer cytoskeletal pathology. Proc Natl Acad Sci 1986; 83: 4913-17.

9. Nukina N, Ihara Y. One of the antigenic determinants of paired helical fi laments is related to tau protein. J Biochem (Tokyo) 1986; 99: 1541-44.

10. Iqbal K, Alonso Adel C, Chen S, et al. Tau pathology in Alzheimer disease and other tauopathies. Biochim Biophys Acta 2005; 1739: 198-210.

11. Farkas E, Luiten PG. Cerebral microvascular pathology in aging and Alzheimer’s disease. Prog Neurobiol 2001; 64: 575-611.

12. Ladecola C. Neurovascular regulation in the normal brain and in Alzheimer’s disease. Nat Rev Neurosci 2004; 5: 347-60.

13. Claassen JA, Jansen RW. Cholinergically mediated augmentation of cerebral perfusion in Alzheimer’s disease and related cognitive disorders: the cholinergic-vascular hypothesis. J Gerontol A Biol Sci Med Sci 2006; 61(3): 267-71.

14. Zlokovic BV. Neurovascular mechanisms of Alzheimer’s neurodegeneration. Trends Neurosci 2005; 28(4): 202-8.

15. Jellinger K. Inverse relation between Braak stage and cerebrovascular pathology in Alzheimer predominant dementia. J Neurol Neurosurg Psychiatry 2000; 68(6): 799-800.

16. Rovelet-Lecrux A, Hannequin D, Raux G, et al. APP locus duplication causes autosomal dominant early-onset Alzheimer disease with cerebral amyloid angiopathy. Nat Genet 2006; 38: 24-6.

17. Sherrington R, Rogaev EI, Liang Y, et al. Cloning of a gene bearing missense mutations in early-onset familial Alzheimer’s disease. Nature 1995; 375: 754-60.

18. Levy-Lahad E, Wasco W, Poorkaj P, et al. Candidate gene for the chromosome 1 familial Alzheimer’s disease locus. Science 1995; 269: 973-77.

19. Corder EH, Saunders AM, Strittmatter WJ, et al. Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer’s disease in late onset families. Science 1993; 261: 921-3.

20. Poirier J, Davignon J, Bouthillier D, Kogan S, Bertrand P, Gauthier S. Apolipoprotein E polymorphism and Alzheimer’s disease. Lancet 1993; 342: 697-9.