Open Access Open Access  Restricted Access Subscription or Fee Access

Nanotechnology: An Antidote for Alzheimer's Disease

Sereene Kaur

Abstract


Alzheimer's disease (AD) is a type of dementia that causes problems with memory, thinking and behaviour. Symptoms usually develop slowly and get worse over time, becoming severe enough to interfere with daily tasks. This article describes different stages of AD along with how it is different from other memory loss issues. Every old-age-related memory loss cannot be AD. Nanotechnology is an emerging branch of science which deals with matter at nanoscale level. Various trails have been proposed to cure AD, but none of them have had positive outcome on humans. Nanoparticles are the only materials that can pass the blood–brain barrier, thus helping in the targeted therapy. None of the medications or vaccinations have ever entered this barrier. Therefore, we have not reached our goal of curing the disease. But with the help of nanoparticles, we can directly target various affected brain parts, without causing any damage to neighbouring cells. The article explains how nanotechnology can be a boom for neurosciences.

Keyword: Alzheimer’s, AD, nanotechnology

Full Text:

PDF

References


D. L. Longo, A. S. Fauci, D. L. Kasper, S. L. Hauser, J. L. Jameson, J. Loscalzo. Harrison’s Principles of Internal Medicine, 18th Edn, Vol. 2; 2011.

R. S. J. Frackowiak, C. Pozzilli, N. J. Legg, G. H. DuBoulay, J. Marshall, G. L. Lenzi, T. Jones. Regional cerebral oxygen supply and utilization in dementia: A clinical and physiological study with oxygen-15 and positron emission tomography, Brain. 1981; 104:753–78p.

M. J. de Leon, S. H. Ferris, A. E. George, B. Reisberg, D. R. Christman, I. I. Kricheff, A. P. Wolf. Computed tomography and positron emission transaxial evaluations of normal aging and Alzheimer’s disease, Journal of Cerebral Blood Flow & Metabolism. 1983; 3:391–4p.

R. Duara, C. L. Grady, J. V. Haxby, M. Sundaram, N. R. Cutler, L. Heston, A. M. Moore, N. L. Schlageter, S. Larson, Si I. Rapoport. Positron emission tomography in Alzheimer’s disease, Neurology. 1986; 36:879–87p.

V. Ibanez, P. Pietrini, G. E. Alexander, M. L. Furey, D. Teichberg, J. C. Rajapakse, S. I. Rapoport, M. B. Schapiro, B. Horwitz. Abnormal metabolic patterns in Alzheimer’s disease after correction for partial volume effects, Neurology. 1998; 50:1585–93p.

P. Pietrini, G. E. Alexander, M. L. Furey, H. Hampel, M. Guazzelli. The neurometabolic landscape of cognitive decline: In vivo studies with positron emission tomography in Alzheimer’s disease, International Journal of Psychophysiology. 2000; 37:87–98p.

S. Minoshima, B. Giordani, S. Berent, K. A. Frey, N. L. Foster, D. E. Kuhl. Metabolic reduction in the posterior cingulate cortex in very early Alzheimer’s disease, Annals of Neurology. 1997; 42:85–94p.

E. M. Reiman, R. J. Caselli, L. S. Yun, K. Chen, D. Bandy, S. Minoshima, S. N. Thibodeau, D. Osborne. Preclinical evidence of a genetic risk factor for Alzheimer’s disease in apolipoprotein E type homozygotes using positron emission tomography. The New England Journal of Medicine. 1996; 334:752–758

W. J. Jagust, R. P. Friedland, T. F. Budinger, E. Koss, B. Ober. Longitudinal studies of regional cerebral metabolism in Alzheimer’s disease, Neurology. 1988; 38:909–12p.

J. V. Haxby, C. L. Grady, E. Koss, B. Horwitz, L. Heston, M. Schapiro, R. P. Friedland, S. I. Rapoport. Longitudinal study of cerebral metabolic asymmetries and associated neuropsychological patterns in early dementia of the Alzheimer type, Archives of Neurology. 1990; 47:753–60.

E. G. McGeer, R. P. Peppard, P. L. McGeer, H. Tuokko, D. Crockett, R. Parks, H. Akiyama, D. B. Calne, B. L. Beattie, R. Harrop. 18fluorodeoxyglucose positron emission tomography studies in presumed Alzheimer cases, including 13 serial scans, Canadian Journal of Neurological Science. 1990; 17:1–11p.


Refbacks

  • There are currently no refbacks.