Dementia of Alzheimer s type

Mishima K, Tozawa T, Satoh K, MatsumotoY, HishikawaY, Okawa M (1999) Melatonin secretion rhythm disorders in patients with senile dementia of Alzheimer s type with disturbed sleep-waking. Biol Psychiatry 45 417-421... 

Iversen LL, Rossor MN, Reynolds GP, Hills R, Roth M, Mountjoy CQ, Foote SL, Morrison JH, Bloom FE (1983) Loss of pigmented dopamine-beta-hydroxylase positive cells from locus coeruleus in senile dementia of Alzheimer s type. Neurosci. Lett. 39 95-100. 

Wilcock GK, Esiri MM, Bowen DM, Hughes AO (1988) The differential involvement of subcortical nuclei in senile dementia of Alzheimer s type. J. Neurol. Neurosurg. Psychiatry 51 842-849. 

Soderberg M., Edlund C., Alafuzoff 1. et al. Lipid composition in different regions of the brain in Alzheimer s disease/senile dementia of Alzheimer s type. J. Neurochem. 1992,5 1646-1653. 

Ejaz Ahmed M, Khan MM, Javed H, Vaibhav K, Khan A, Tabassum R et al (2013) Amelioration of cognitive impairment and neurodegeneration by catechin hydrate in rat model of streptozotocin-induced experimental dementia of Alzheimer s type. Neurochem Int 62 492-501... 

Adolfsson, R., Gottfries, C.G., Roos, B.E. and Winblad, B. (1979) Changes in the brain catecholamines in patients with dementia of Alzheimer s type. Br. J. Psychiatry 135 216-223. 

By 1989, about 2000 individuals in the Minamata area have been officially certified to have Minamata Disease and eligible for financial compensation. Histopathologi-cal changes in brain were clearly linked to organomercury insult in Minamata Disease victims and the distribution of lesions in the nervous system was characteristic, especially in the cerebral cortices and the cerebellum. Pathological studies of 112 Minamata Disease victims also showed elevated frequencies of sepsis and malignant neoplasms of the thyroid gland when compared to 112 sex-age matched pair control deaths between 1970 and 1983 from various causes (senile dementia of Alzheimer s type, Parkinson s disease of idiopathic type, amyotrophic lateral sclerosis) in western parts of Japan. 

Meador, K., Loring, D., Nichols, M., Zamrini, E., Rivner, M., Posas, H., Thompson, E., and Moore, E., 1993. Preliminary findings of high-dose thiamine in dementia of Alzheimer s type. Journal of Geriatric Psychiatry and Neurology. 6 222-229. 

McCaddon, A., Davies, G., Hudson, P., Tandy, S., and Cattell, H., 1998. Total serum homocysteine in senile dementia of Alzheimer s type. International Journal of Geriatric Psychiatry. 13 235-239. 

The recommended initial dose of memantine hydrochloride for the treatment of moderate to severe dementia of Alzheimer s type is 5 mg orally once daily. The dose should be increased in 5 mg increments to 10 mg/day (given as 5 mg twice daily), 15 mg/day (given twice daily in separate doses of 5 mg and 10 mg), and 20 mg/day (given as 10 mgtwice daily). The minimum recommended interval between dose increases is 1 week. The recommended maintenance dose is 10 mg twice daily (20 mg/day). There is not an established dose for the treatment of chronic pain states, but case reports and medication trials have started at 5-10 mg BID and increases at 1 week intervals to 30 mg/day have been examined [3-5]. 

Soderberg M, Edlund C, Alafuzoff I, Kristensson K, Dallner G. lipid composition in different regions of the brain in Alzheimer s disease/senile dementia of Alzheimer s type. J Neurochem. 1992 59(5) 1646-1653. Svennerholm L, Gottfries CG. Membrane Upids, selectively diminished in Alzheimer brains, suggest synapse loss as a primary event in early-onset form (t)fpe I) and demyelinationin late-onset form (t)fpe II). / Neurochem. 

However, neuropathological examination in three patients with temporal lobe atrophy and vascular dementia found no evidence of Alzheimer s type pathology in the cortex (Fein et al. 2000). Therefore, medial temporal lobe atrophy is not specific to Alzheimer s dementia. However, it maybe of some discriminatory value in early disease (Jobst et al. 1998 O Brien et al. 2000), although this may be less so in elderly patients in whom medial temporal lobe atrophy may simply reflect age-related cerebral atrophy. 

Other nootropic agents in some stage of clinical development include nebracetam (9), nefinacetam (10), and BMY 21502 (11). Nebracetam, an aminomethyl pyrrolidinone derivative, is expected to be approved in Japan in 1994 (73). In clinical studies involving patients having cerebrovascular or senile dementia of the Alzheimer s type, clinical symptoms such as spontaneous or emotional expression were enhanced in up to 71% of cases. Long-term treatment using nebracetam in patients with cerebral infarction also afforded marked improvement in most cases with few side effects (74). A review of this compound has beenpubUshed (75). 

AD is the most common type of dementia, affecting approximately 4.5 million Americans in the year 2000.2 Table 32-2 lists the different classifications of dementia.3 This chapter will address only dementia of the Alzheimer s type. 

Dementia of the Alzheimer s type (early- or late-onset)... 

The ChE inhibitors all have the indication for the treatment of mild to moderate dementia of the Alzheimer s type. Guidelines for the treatment of AD were written before the approval of memantine and recommend the use of ChE inhibitors as a valuable treatment for AD.27-29 None of the ChE inhibitors have been compared in head-to-head studies, so the decision to use one over another is based on differences in mechanisms of action, adverse reactions, and titration schedules. 

Donepezil is approved for the treatment of mild to moderate dementia of the Alzheimer s type at a dose of 5 mg/day. This dose should be increased to 10 mg/day if needed after 4 to 6 weeks. Table 32-5 describes the dosing strategies for all of the approved agents for Alzheimer s disease.34-38... 

A possible answer comes unexpectedly from experiments originally aimed at investigating the role of the pre-senilin-1 gene, whose mutations lead to familial early-onset Alzheimer s disease. This type of Alzheimer s disease is known to be the most aggressive form that can cause severe memory loss and dementia in patients as early as in their 30s. Recent studies have shown that forebrain-specific... 

The first neurochemical evidence of a disturbed serotonin function in cognition came from the changes in serotonin and/or 5-hydroxyindoleacetic acid (5-HIAA) levels in a number of forebrain nuclei, the temporal and cingulate cortex, hippocampus, and other areas of the brain taken at autopsy from patients with senile dementia of the Alzheimer s type (Adolfsson et al. 1978 Arai et al. 1984 D. M. Bowen et al. 1979, 1983 A. J. Cross et al. 1983 Winblad et al. 1982). The depletions are regionally selective reductions in se-... 

Similar results were obtained from material taken from patients with senile dementia of the Alzheimer s type (Chan-Palay et al. 1992). A loss of tryptophan hydroxylase immunoreactive neurons in the raphe nuclei, which was most pronounced in the lateral division, was correlated with both age and cortical pathology. Furthermore, tyrosine hydroxylase reactive neurons were also found to be reduced in the locus coeruleus, even more so than the tryptophan hydroxylase reactive neurons. The same was also found for material taken from brains with Parkinson s disease. 

Hong J-S, Tilson HA, Yoshikawa K Effects of lithium and haloperidol administration on the rat brain levels of Substance P. J Pharmacol Exp Ther 224 590-597, 1983 Honig A, Bartlett JR, Bouras N, et al Amino acid levels in depression a preliminary investigation. J Psychiatr Res 22 159-164, 1989 Honjo H, Ogino Y, Natitoh K, et al In vivo effects by estrone sulphate on the central nervous system on senile dementia [Alzheimer s type). Journal of Steroid Biochemistry 34 521-525, 1989... 

Nemeroff CB, Krishnan KRR, Reed D, et al Adrenal gland enlargement in major depression a computed tomographic study. Arch Gen Psychiatry 49 384-387, 1992 Nestler EJ, Terwilliger RZ, Duman RS Chronic antidepressant administration alters the subcellular distribution of cyclic AMP-dependent protein kinase in rat frontal cortex. J Neurochem 53 1644-1647, 1989 Nestor PC, Parasuraman R, Haxby JV, et al Divided attention and metabolic brain dysfunction in mild dementia of the Alzheimer s type. Neuropsychologia 29(5) 379-387, 1991... 

Prince DA, Wilder BJ Cortical mechanisms in cortical epileptogenic foci surrounded inhibition. Arch Neurol 16 194-202, 1967 Prinz PN, Vitahano PP, Vitiello MV, et al Sleep, EEC and mental function changes in senile dementia of the Alzheimer s type. Neurobiol Aging 3 361-370, 1982... 

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