Biologic Markers in Alzheimer's Disease

Thienhaus, Ole J.; Hartford, James T.; Skelly, Michael F.; Bosmann, H.Bruce

doi:10.1111/j.1532-5415.1985.tb01782.x

Cited by 15 publications

(8 citation statements)

References 87 publications

(101 reference statements)

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“…The different roles of different types of 5-HT receptor make it unlikely, however, that any simple relationships will emerge (Lawlor et al, 1989). Good reviews of serotonergic function in dementia are given by Whitford (1986) and Thienhaus et al (1985). If reduced 5-HT levels in the brain are one cause of aggressive behaviour in dementia then drugs which increase 5-HT functioning might be expected to reduce such behaviour.…”

Section: Biological Factorsmentioning

confidence: 99%

Aggressive behaviour in elderly people with dementia: A review

Patel

Hope

1993

Int J Geriat Psychiatry

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SUMMARYThe progressive degeneration of the brain seen in dementia is often accompanied by behaviourai disturbances. Aggressive behaviour is one of the most serious of these disturbances and is a common cause for psychiatric referral, admission to hospital and drug treatment. In this article, we discuss the conceptual issues associated with defining aggressive behaviour in cognitively impaired patients. We then review the aetiology, epidemiology, methods of assessment, and management of aggressive behaviour in elderly people with dementia.

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Section: Biological Factorsmentioning

confidence: 99%

Aggressive behaviour in elderly people with dementia: A review

Patel

Hope

1993

Int J Geriat Psychiatry

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“…IGF-I appears to have important actions on neuronal survival, glial differentiation, maintenance of the bloodbrain bamer, and other processes that may be affected in Alzheimer's disease and chronic alcoholism. Both Alzheimer's disease and chronic alcohol abuse are known to cause cerebral cortical and hippocampal pathology, including neurotransmitter receptor losses (Thienhaus et al, 1985;Reubi and Palacios, 1986;Ballinger, 1988a, 1989u,b).…”

mentioning

confidence: 99%

Insulin‐Like Growth Factor I Receptor Binding in Brains of Alzheimer's and Alcoholic Patients

Crews

McElhaney

Freund

et al. 1992

Journal of Neurochemistry

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Patients with chronic alcoholism and/or Alzheimer's disease show degenerative changes in the cerebral cortex and hippocampus. To investigate possible changes in insulin-like growth factor I receptor binding sites in brain tissue of patients with these pathological conditions, the number of 125I-insulin-like growth factor I binding sites was determined in tissues obtained from control patients and those with Alzheimer's and/or with a history of alcoholism. The four experimental groups examined consisted of patients from similar age groups. Postmortem histology and a clinical history were used for the diagnosis of Alzheimer's disease and alcoholism, respectively. Careful clinical records were kept concerning other variables such as immediate cause of death and medications administered before death. Specific binding of 125I-insulin-like growth factor I to homogenates prepared from cerebral cortex of Alzheimer's, alcoholic, alcoholic Alzheimer's, and age-matched control patients was similar, although Alzheimer's patients tended to have slightly higher binding values. No significant differences in insulin-like growth factor I binding in cerebral cortex were found with regard to age of patients, the interval between death and autopsy, and CNS-active medications. No statistical differences in 125I-insulin-like growth factor I binding were noted in hippocampal tissue from the four patient groups. Thus, human insulin-like growth factor I binding sites in cerebral cortex and hippocampus appear unaffected by several variables.

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“…Cholinergic neurons are lost in the central nervous system above and beyond what is seen in normal aging 4 – 11 . Vasopressin has also been evaluated, 9 , 12 – 21 since it has been thought to play a role in memory. Vasopressin is released from the hypothalamus in response to the level of serum osmolality and also in response to a variety of other stimuli including plasma volume, blood pressure, pain, nausea, and emotional factors.…”

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confidence: 99%

Vasopressin Response to Dehydration in Alzheimer's Disease

Albert¹,

Nakra²,

Grossberg³

et al. 1989

J American Geriatrics Society

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Alzheimer's disease is a progressive deterioration of neuropsychological functioning. One of the main neuropathological correlates of the disease is a drop-out of cholinergic neurons within the central nervous system. The neuropeptide that is responsible for water homeostasis and defense against dehydration, vasopressin, is also under direct cholinergic control. Several studies have suggested that in Alzheimer's disease there has been a trend toward lower vasopressin levels than in age-matched controls. In order to improve discrimination of normal from diminished vasopressin levels, nine subjects with Alzheimer's disease (mean age 65 +/- 2 years) and nine age- and sex-matched controls (68 +/- 3 years) underwent a mild provocative challenge of overnight fluid restriction. Individuals with Alzheimer's disease had a greater degree of dehydration, with overnight serum osmolality of 313 +/- 4 vs 300 +/- 3 Mosmol/kg, P = .01, and diminished "thirst" as measured by water ingested in one hour of ad libitum water intake. Eight of the nine with Alzheimer's disease had levels of vasopressin which, by extrapolation, appear to be subnormal for their serum osmolalities, whereas seven of the nine control subjects has vasopressin levels within or above the reference range (P less than .05). Elderly individuals with Alzheimer's disease may be at increased risk of dehydration during periods of fluid restriction due to the loss of normal physiological responses of "thirst" and vasopressin secretion.

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Biologic Markers in Alzheimer's Disease

Cited by 15 publications

References 87 publications

Aggressive behaviour in elderly people with dementia: A review

Aggressive behaviour in elderly people with dementia: A review

Insulin‐Like Growth Factor I Receptor Binding in Brains of Alzheimer's and Alcoholic Patients

Vasopressin Response to Dehydration in Alzheimer's Disease

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