By Khalid Iqbal, Sangram S. Sisodia, Bengt Winblad
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Additional resources for Alzheimer z disease advances in etiology, pathogenesis a therapeutics
Dr Frangione then postulated that: (1) in FAD genetic mutations are responsible for different phenotypic expressions; and that (2) the precursor of amyloid (as in different types of systemic and localized amyloidosis) is present in the circulation. Dr Frangione demonstrated in 1990 that in Dutch patients, the gene coding for the amyloid precursor protein (APP) contained a point mutation. This work provided an enormous stimulus to look for mutations in other amyloidosis and established a rationale for examination of mutations of the APP gene in pedigrees of FAD.
3). CONCLUSIONS . Episodic memory deficits are dominant in both early clinical and preclinical phases of AD. These deficits in preclinical AD are generalizable across various dimensions of episodic memory. Preclinical episodic memory deficits may be seen several years (six to ten) before diagnosis, but the degree of impairment appears stable up until the period more closely preceding diagnosis. In addition to cognitive assessment, other markers such as family reports, depressive symptoms, and paraclinical examinations may help in identifying subjects in the preclinical phase of AD.
Neurology, 45, 1161–8. se Alzheimer’s Disease: Advances in Etiology, Pathogenesis and Therapeutics Edited by Khalid Iqbal, Sangram S. Sisodia and Bengt Winblad Copyright & 2001 John Wiley & Sons Ltd Print ISBN 0-471-52176-0 Online ISBN 0-470-84645-3 2 Epidemiology of Alzheimer’s Disease and Dementia: Advances and Challenges ROBERT KATZMAN INTRODUCTION A defining event of the twentieth century was the dramatic increase in life expectancy at birth—an increase of over 50%, from under age 50 in 1900 to over age 76 in 2000.
Alzheimer z disease advances in etiology, pathogenesis a therapeutics by Khalid Iqbal, Sangram S. Sisodia, Bengt Winblad