Cognitive impairment in Alzheimer’s disease

Frydman-Marom, A., Levin, A., Farfara, D., Benromano, T., Scherzer-Attali, R., Peled, S., and Ovadia, M. 2011. Orally administrated cinnamon extract reduces p-amyloid oligomerization and corrects cognitive impairment in Alzheimer s disease animal models. PloS One, 6(1), el6564. 

Perry EK, Curtis M, Dick DJ, et al Chohnergic correlates of cognitive impairment in Parkinson s disease comparisons with Alzheimer s disease. J Neurol Neurosurg Psychiatry 48 413-421, 1985... 

Terry, R. D., Masliah, E., Salmon, D. P., Butters, N., DeTeresa, R., Hill, R., Hansen, L. A., and Katzman, R. (1991). Physical basis of cognitive alterations in Alzheimer s disease synapse loss is the major correlate of cognitive impairment. Ann Neurol 30, 572-580. 

Ghoshal N, Garcia-Sierra F, Wuu J, Leurgans S, Bennett DA, et al. 2002. Tau conformational changes correspond to impairments of episodic memory in mild cognitive impairment and Alzheimer s disease. Exp Neurol 177 475-493. 

Traykov L, Rigaud AS, Baudic S, Smagghe A, Boiler F, Forette F (2002) Apohpoprotein E epsilon 4 allele frequency in demented and cognitively impaired patients with and without cerebrovascular disease. J Neurol Sci 203-204 177-181 Vanhanen M, Soininen H (1998) Glucose intolerance, cognitive impairment and Alzheimer s disease. Curr Opin Neurol 11 673-677... 

Terry RD, et al. Physical basis of cognitive alterations in Alzheimer s disease synapse loss is the major correlate of cognitive impairment. Ann. Neurol. 1991 30 572-80. 

Ahmed, N., Ahmed, U., Thornalley, P. J., Hager, K., Fleischer, G., and Munch, G. (2005). Protein glycation, oxidation and nitration adduct residues and free adducts of cerebrospinal fluid in Alzheimer s disease and link to cognitive impairment. ]. Neurochem. 92, 255-263. 

The concept of bradyphrenia overlaps with that of apathy, defined as diminished motivation not attributable to diminished level of consciousness, cognitive impairment or emotional distress (Marin, 1990). Apathy is common in neurodegenerative disorders and is associated with orbito-frontal, medial frontal and anterior temporal dysfunction in Alzheimer s disease (Craig et al., 1996). Apathy is one of the most common neuropsychiatric symptoms in PD, and correlates with executive dysfunction (Aarsland, 1999b). However, apathy is even more common in PSP patients (Aarsland et al., 2001c), possibly related to the more marked involvement of the orbitofrontal and medial frontal circuits in PSP than in PD. 

A decline in trophic factors may contribute to aging, and a reduced level of hippocampal 5-HT, receptors in Alzheimer s disease would lead to decreased release of S-100 and increased levels of S-100 within cells (Griffin et al. 1989). The relevance of such changes to neuronal cell loss in the hippocampus and cortex remains to be established. The possibility that other serotonin receptor subtypes may also regulate the release of trophic factors remains to be determined (Whitaker-Azmitia and Azmitia 1991], as does the search for other neuronal growth factors (Zhou and Azmitia 1991]. However, such factors and the involvement of serotonin in their release may subsequently be shown to afford a site of drug action to attenuate cell decline and cognitive impairment. 

Butterfield DA, Sultana R. 2007. Redox proteomics identification of oxidatively modified brain proteins in Alzheimer s disease and mild cognitive impairment Insights into the progression of this dementing disorder. J Alzheimers Dis 12 61-72. 

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