Senile Dementia; A Clinical Study of Two Hundred Cases With Particular Regard to Types of the Disease

Pickett, William

doi:10.1097/00005053-190402000-00002

Cited by 10 publications

(5 citation statements)

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“…Alzheimer himself suffered kidney failure in the last few weeks of his short life; he too may have used PN to excess [ 8 ]. The recognition of senile dementia as a consequence of nephritis in an unspecified number of patients may have been an error of interpretation but not of clinical observation [ 37 ]. Chronic forms of nephritis were recorded in a series of 16 dementia patients who displayed plaques with or without tangles [ 57 ].…”

Section: Pn: Nephrotoxicity and F-admentioning

confidence: 99%

The Alzheimer Pandemic: Is Paracetamol to Blame?

Jones¹

2014

IADT

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Historical Background: The clinical recognition of a form of dementia closely resembling Alzheimer's disease dates from around 1800. The role of analgesics derived from coal-tar in the spread of the pandemic is traced in terms of the introduction of phenacetin (PN) in 1887; its nephrotoxicity; the observation of lesions characteristic of the disease by Fischer and Alzheimer; the discovery of paracetamol (PA) as the major metabolite of PN; the linking of kidney injury and dementia with high PN usage; and the failure of PN replacement by PA to halt and reverse the exponential, inexorable rise in the incidence of Alzheimer-type dementia. Fischer observed his first case before Alzheimer; it is proposed to rename the syndrome Fischer-Alzheimer disease (F-AD).Disease development: PA-metabolising enzymes are localised in the synaptic areas of the frontal cortex and hippocampus, where F-AD lesions arise. The initiating chemical lesions in liver poisoning comprise covalent binding of a highly reactive product of PA metabolism to proteins; similar events are believed to occur in brain, where alterations in the antigenic profiles of cerebral proteins activate the microglia. β-Amyloid forms, and, like PA itself, induces nitric oxide synthase. Peroxynitrite modifies cerebral proteins by nitrating tyrosine residues, further challenging the microglia and exacerbating the amyloid cascade. Spontaneous reinnervation, N-acetyl cysteine administration and tyrosine supplementation may attenuate the early stages of F-AD development.Conclusion: F-AD is primarily a man-made condition with PA as its principal risk factor.

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Section: Pn: Nephrotoxicity and F-admentioning

confidence: 99%

The Alzheimer Pandemic: Is Paracetamol to Blame?

Jones¹

2014

IADT

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“…At the beginning of the century Pickett (1904) proposed a distinction between Delirium and confusion in elderly people, believing that Delirium always has an organic cause while confusion could be caused by other nonorganic factors. A few years later Bonhoeffer described acute organic brain disorders as 'symptomatic psychoses' which included simple Delirium, hallucinosis, amentia, 'epileptic type' and symptomatic stupor, all of which were characterized by clouding of consciousness.…”

Section: Twentieth Centurymentioning

confidence: 99%

A brief review of the history of delirium as a mental disorder

et al. 2007

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“…Research in this age group became important for it avoided the problem of having to decide whether the brain lesions were related to primary states of mania or melancholia. By the early 1900s efforts had also been made to: (a) measirre the symptoms and severity of dementia (Jaspers, 1910;Puillet and Morel, 1913;Berrios, 1990); (b) ascertain the differential importance of the senile and vascular aetiology of dementia (McGafin, 1910;Treadway, 1913); and (c) study the comparative prevalence of senile dementia in relation to other psychiatric disorders affecting the elderly (Pickett, 1904;Southard, 1910;Bolton, 1903). These enquiries were influenced by ongoing theories on ageing of brain tissue (Marinesco, 1900).…”

Section: History Of the Notion Of Dementiamentioning

confidence: 99%