Alzheimer’s dementia

Maelicke A., and Albuquerque, E. X. (1996). New approach to drug therapy of Alzheimer s dementia. Drug Discovery Today 1 53-59. 

Evans, P.H., Klinowski, J. and Yano, E. (1991). Cephaloconi-osis a free radical perspective on the proposed particulate-induced etiopathogenesis of Alzheimer s dementia and related disorders. Med. Hypoth. 34, 209-219. 

Evans, P.H., Peterhans, E., Biirge T. and Klinowski, J. (1992b). Aluminosilicate-induced free radical generation by murine brain glial cells in vitro potential significance in the etiopathogenesis of Alzheimer s dementia. Dementia 3, 1-6. 

Evans, P.H., Yano, E., Klinowski, J. and Peterhans, E. (1992c). Oxidative damage in Alzheimer s dementia, and the potential etiopathogenic role of aluminosilicates, microglia and micronutrient interactions. In Free Radicals and Aging (eds. I. Emerit and B. Chance) pp. 178-189. Birkhauser, Basel. 

Father died at age 85 with Alzheimer s dementia mother died at age 86 with history of colon cancer and osteoporotic fractures of the hip and spine brother alive and well at age 71. SH... 

Even in Alzheimer s disease (AD), the possible involvement of a weak excitotoxic process cannot be ruled out. Indeed, mitochondrial abnormalities (such as cytochrome oxidase alterations) [36, 37] and increased levels of markers of oxidative stress [38] have been reported in AD. This has been the rationale for testing the NMDA antagonist memantine in Alzheimer s dementia [39]. 

Juhasz A, Rimanoczy A, Boda K, Vincze G, Szlavik G, et al. 2005. CYP46 T/C polymorphism is not associated with Alzheimer s dementia in a population from Hungary. Neu-rochem Res 30 943-948. 

Reiman, E.M., Chen, K., Alexander, G.E., et al. (2004) Eunctional brain abnormaUties in young adults at genetic risk for late-onset Alzheimer s dementia. Proc. Natl. Acad. Sci. U. S. A., 101, 284-289. 

Zuliani, G., Ble, A., Zanca, R., et al. (2001) Genetic polymorphisms in older subjects with vascular or Alzheimer s dementia. Acta Neurol. Scand., 103,304-308. 

Chapman, J., Wang, N., Treves, T.A., Korczyn, A.D., Borstein, N.M. (1998) ACE, MTHFR, factor V Leiden, and APOE polymorphisms in patients with vascular and Alzheimer s dementia. Stroke, 29, 1401-1404. 

Increasing Oxygen. It was once believed that the cause of Alzheimer s dementia was poor oxygen snpply to the brain. This theory suggested that atherosclerosis, hard plaques of fat and calcium, accumulate in blood vessels and block the arteries that snpply the brain, depriving it of oxygen-rich blood. In fact, atherosclerosis does occnr in the carotid arteries that snpply the brain and is the most common cause of stroke and vascnlar dementia. There is no evidence that this mechanism is involved in the pathology of Alzheimer s disease. 

Chelation. Chelation (pronounced KEY-lay-shnn) medications act by removing trace metals from the body. They are used most often in cases of accidental or intentional overdose of substances containing these elements. Chelators have been used to treat dementia based on evidence that patients with Alzheimer s dementia have abnormally high levels of aluminum in their nerve cells. It s not clear why this may occnr. As a resnlt, chelating medications snch as desferrioxamine have been... 

Most of the other medications studied to slow the course of Alzheimer s dementia presumably work as an antioxidant to protect nerve cells from damaging free radicals. Of the antioxidants, vitamin E is the safest and has the best evidence of efficacy. Thus, we recommend that all patients receive 2000 lU of vitamin E each day during... 

Palo J, Palmer AM, Neary D, Bowen DM, Wikstrom J, Davison AN, Sims NR. (1984) Monoamine metabolite concentrations in lumbar cerebrospinal fluid of patients with histologically verified Alzheimer s dementia. J Neurol Neurosurg Psychiatry 47 481 84. 

Medical illness or medication side effects may directly affect cognition virtually all classes of medication have been implicated. In adult patients, glucocorticoids can impair memory at relatively low doses (Keenan et ah, 1995 Newcomer et ah, 1999), as there are postulated effects on hippocampal neurons. Newcomer et ah, (1999) have reviewed the literature on illnesses in adults in which memory inversely correlates with cortisol levels, such as in Cushing s disease, Alzheimer s dementia, schizophrenia, and depression. There is no similar literature on the pediatric population. The risk of memory impairment puts chronic steroid treatment, such as that seen in certain pediatric rheumatologic disorders and severe asthmatics, for example, into a different perspective, however. Documentation of memory both before and during chronic steroid treatment might help determine detrimental effects in the pediatric population. 

Mouradian MM, Bhn J, Giuffra M Somatostatin replacement therapy of Alzheimer s dementia. Ann Neurol 30 610-613, 1991... 

Protein misfolding diseases (Alzheimer s dementia, prion diseases)... 

The Clinical-Molecular Interface Alzheimer s Dementia as a Cholinergic Disorder... 

It is indicated in arteriosclerotic dementia, primary progressive dementia, Alzheimer s dementia, multiinfarct dementia and primary progressive dementia. 

Some of the expected changes with age, such as the reduction in cholinergic neurons or the presence of Alzheimer s dementia, may accentuate the anticholinergic effects of many antipsychotics and antidepressants. Thus, elderly patients have increased sensitivity to these properties, often resulting in a central anticholinergic syndrome (267). This condition is characterized by the loss of immediate memory, confusion, disorientation, and florid visual hallucinations, at times superimposed on other psychoses, such as schizophrenia or psychotic depression. 

More recently, 206 nursing home patients with moderate to severe Alzheimer s dementia with behavior disturbances or psychosis were randomly assigned to either placebo or a fixed dose of olanzapine at 5, 10, or 15 mg per day for up to 6 weeks of treatment ( 285). In this multicenter, double-blind, placebo-controlled study, olanzapine was significantly more efficacious than placebo in reducing psychosis and behavioral disturbances. The best result was obtained with the 5-mg dose in patients who did not have delusions or hallucinations. Although these patients were selected because of behavioral disturbance, hallucinations, or delusions, 75% did not have hallucinations at baseline, 43% did not have delusions at baseline, and 38% did not have psychosis at baseline. At end point, of those patients without hallucinations at baseline, hallucinations developed in 7.4% on olanzapine, compared with 21.9% on placebo ( p = 0.045). For those without delusions, 17% of placebo patients and 4% of olanzapine patients experienced delusions. For those subjects without psychosis (i.e., neither hallucinations nor delusions), psychosis developed in 8% of olanzapine patients and 25% of placebo patients (p = 0.006). Thus, olanzapine also seemed to prevent the occurrence of psychotic symptoms as the disease progressed. 

Dihydroergotoxine, a mixture of dihydro-K-ergocryptine and three similar dihydrogenated peptide ergot alkaloids (ergoloid mesylates), has been promoted for many years for the relief of senility and more recently for the treatment of Alzheimer s dementia. There is no useful evidence that this drug has significant benefit. 

Those disorders that require the presence of psychosis (Table 10—1) as a defining feature of the diagnosis include schizophrenia, substance-induced (i.e., drug-induced) psychotic disorder, schizophreniform disorder, schizoaffective disorder, delusional disorder, brief psychotic disorder, shared psychotic disorder, and psychotic disorder due to a general medical condition. Disorders that may or may not have psychotic symptoms (Table 10—2) as an associated feature include mania and depression as well as several cognitive disorders such as Alzheimer s dementia. 

Ergoloid is a psychotherapeutic agent that is indicated in the treatment of age-related decline in mental capacity, primary progressive dementia, Alzheimer s dementia, multi-infarct dementia, and senile onset. Ergoloid is thought to increase cerebral blood flow. 

Teunissen CE, de Vente J, Steinbusch HW, De Bruijn C. Biochemical markers related to Alzheimer s dementia in serum and cerebrospinal fluid. Neurobiol Aging 2002 23 485-508. 

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