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Living with Dementia

Alzheimer’s disease

  • - Dementia: general aspects
  • Jun 20, 2011
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Tags: | alzheimer | alzheimer's disease | bonfiglio | concept of dementia |

AD has become the prototypical form of dementia. From this point of view, a study of its origins should throw light on the evolution of the concept of dementia. The writings of Alzheimer, Fischer, Fuller, Lafora, Bonfiglio, Perusini, Ziveri, Kraepelin and other protagonists are deceptively fresh, and this makes anachronistic reading inevitable.  However,  the psychiatry of the late nineteenth century is a remote country: concepts such as dementia, neurone, neurofibril and plaque were then still in process of construction and meant different things to different people. A discussion of these issues is beyond the scope of this section (for this see Berrios, 1990b). THE NEUROPATHOLOGY OF DEMENTIA BEFORE ALZHEIMER
Enquiries into the brain changes accompanying dementia started during the 1830s but consisted in descriptions of external appearance (Wilks, 1865). The first important microscopic study was that of Marce (1863) who described cortical atrophy, enlarged ventricles and ‘softening’. The vascular origin of softening was soon ascertained (Parrot, 1873), but the distinction between vascular and parenchymal factors had to await until the 1880s. From then on, microscopic studies concentrated on cellular death, plaques and neurofibrils. ALZHEIMER AND HIS DISEASE
Alzheimer (1907) reported the case of a 51-year-old woman, with cognitive impairment, delusions, hallucinations, focal symptoms,  and whose brain showed plaques,  tangles and arteriosclerotic changes.

The existence of neurofibrils had been known for some time (DeFelipe and Jones, 1988); for example, that in senile dementia ‘the destruction of the neurofibrils appears to be more extensive than in the brain of a paralytic subject’ (Bianchi 1906, p. 846). Fuller (1907)  had remarked in June 1906 (i.e. five months before Alzheimer’s report)  on the presence of neurofibrillar bundles in senile dementia (p. 450). Likewise, the association of plaques with dementia was not a novelty: Beljahow (1889) had reported them in 1887, and so had Redlich and Leri few years later (Simchowicz, 1924); in Prague, Fischer (1907) gave an important paper in June 1907 pointing out that miliary necrosis could be considered as a marker of senile dementia.

Nor was the syndrome described by Alzheimer new: states of persistent cognitive impairment affecting the elderly, accompanied by delusions and hallucinations were well known (Marce,  1863;  Krafft-Ebing,  1873;  Crichton-Browne,  1874; Marie, 1906). As a leading neuropathologist Alzheimer was aware of this work. Did he then mean to describe a new disease?

The answer is that it is most unlikely he did, his only intention having been to point out that such a syndrome could occur in younger people (Alzheimer, 1911). This is confirmed by commentaries from those who worked for him: Perusini (1911) wrote that for Alzheimer ‘these morbid forms do not represent anything but atypical form of senile dementia’ (p. 143). THE NAMING OF THE DISEASE
Kraepelin (1910)  coined the term in the 8th edition of his Handbook: at the end of the section on ‘senile dementia’ he wrote:

the autopsy revels,  according to Alzheimer’s description,
changes that represent the most serious form of senile demen-
tia ... the Drusen were numerous and almost one third of the
cortical cells had died off.  In their place instead we found
peculiar deeply stained fibrillary bundles that were closely
packed to one another, and seemed to be remnants of degen-
erated cell bodies ... The clinical interpretation of this AD is
still confused. Whilst the anatomical findings suggest that we
are dealing with a particularly serious form of senile demen-
tia, the fact that this disease sometimes starts already around
the age of 40 does not allow this supposition. In such cases we
should at least assume a ‘senium praecox’ if not perhaps a more
or less age-independent unique disease process.

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Alzheimer’s Disease

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