A Comparison of Early-Onset and Late-Onset Depressive Illness in the Elderly

1989 ◽  
Vol 155 (5) ◽  
pp. 673-679 ◽  
Author(s):  
P. W. Burvill ◽  
W. D. Hall ◽  
H. G. Stampfer ◽  
J. P. Emmerson

Elderly patients with early-onset and late-onset depressive illness presenting to psychiatrists for treatment were compared for social, demographic, and clinical measures. For most factors measured no statistically significant differences were found. In the early-onset cases, patients were significantly more severely depressed. There was some evidence for the hypotheses that family history is less important and biological factors more important in late-onset depression. It is suggested that the latter hypothesis should be tested by a range of the newer neuroanatomical and neurophysiological laboratory investigations. The findings indicate that neuroticism is an important underlying factor in both early-onset and late-onset depression in the elderly.

1989 ◽  
Vol 155 (05) ◽  
pp. 673-679 ◽  
Author(s):  
P. W. Burvill ◽  
W. D. Hall ◽  
H. G. Stampfer ◽  
J. P. Emmerson

Elderly patients with early-onset and late-onset depressive illness presenting to psychiatrists for treatment were compared for social, demographic, and clinical measures. For most factors measured no statistically significant differences were found. In the early-onset cases, patients were significantly more severely depressed. There was some evidence for the hypotheses that family history is less important and biological factors more important in late-onset depression. It is suggested that the latter hypothesis should be tested by a range of the newer neuroanatomical and neurophysiological laboratory investigations. The findings indicate that neuroticism is an important underlying factor in both early-onset and late-onset depression in the elderly.


1983 ◽  
Vol 28 (2) ◽  
pp. 102-104 ◽  
Author(s):  
Martin G. Cole

Thirty-eight elderly patients with primary depressive illness (Feighner criteria) were followed up for 7–31 months. In the absence of persistent organic signs and severe physical illness, age of onset (first depressive episode after 60) but not age was significantly related to course of illness. Compared to early onset depressives, late onset depressives were more likely to remain completely well during the follow-up period and less likely to have frequent or disabling relapses.


2020 ◽  
Vol 9 (11) ◽  
pp. 3665
Author(s):  
Dongmin Kim ◽  
Pil-Sung Yang ◽  
Gregory Y.H. Lip ◽  
Boyoung Joung

Atrial fibrillation (AF) is considered a risk factor for dementia, especially in the elderly. However, the association between the two diseases is not well identified in different age subgroups. The association of incident AF with the development of dementia was assessed from 1 January 2005, to 31 December 2013, in 428,262 participants from a longitudinal cohort (the Korea National Health Insurance Service-Health Screening cohort). In total, 10,983 participants were diagnosed with incident AF during the follow-up period. The incidence of dementia was 11.3 and 3.0 per 1000 person-years in the incident-AF and without-AF groups, respectively. After adjustment for clinical variables, the risk of dementia was significantly elevated by incident AF, with a hazard ratio (HR) of 1.98 (95% confidence interval [CI]: 1.80–2.17, p < 0.001), even after censoring for stroke (HR: 1.74, 95% CI: 1.55–1.94, p < 0.001). The HRs of incident AF for dementia onset before the age of 65 (early-onset dementia) and for onset after the age of 65 (late-onset dementia) were 2.91 (95% CI: 1.93–4.41) and 1.67 (95% CI: 1.49–1.87), respectively. Younger participants with AF were more prone to dementia development than older participants with AF (p for trend < 0.001). AF was associated with an increased risk of both early- and late-onset dementia, independent of clinical stroke.


2004 ◽  
Vol 184 (6) ◽  
pp. 488-495 ◽  
Author(s):  
Adrian J. Lloyd ◽  
I. Nicol Ferrier ◽  
Robert Barber ◽  
Anil Gholkar ◽  
Allan H. Young ◽  
...  

BackgroundEvidence for structural hippocampal change in depression is limited despite reports of neuronal damage due to hypercortisolaemia and vascular pathology.AimsTo compare hippocampal and white matter structural change in demographically matched controls and participants with early-onset and late-onset depression.MethodHigh-resolution volumetric magnetic resonance imaging (MRI) and rating of MRI hyperintensities.ResultsA total of 51 people with depression and 39 control participants were included. Participants with late-onset depression had bilateral hippocampal atrophy compared with those with early-onset depression and controls. Hippocampal volumes did not differ between control participants and those with early-onset depression. Age of depression onset correlated (negatively) with hippocampal volume but lifetime duration of depression did not. Hyperintensity ratings did not differ between groups.ConclusionsResults suggest that acquired biological factors are of greater importance in late-than in early-onset illness and that pathological processes other than exposure to hypercortisolaemia of depression underlie hippocampal atrophy in depression of late life.


1981 ◽  
Vol 139 (5) ◽  
pp. 463-466 ◽  
Author(s):  
J. Mendlewicz ◽  
M. Baron

SummaryDespite the high prevalence of unipolar depression in the general population, few genetic studies are available on subtypes of unipolar illness. We evaluated morbid risks for depression, alcoholism and/or sociopathy in the relatives of early onset (before age 40) and late onset (after age 40) unipolar patients in a sample of 106 probands consecutively admitted to the New York State Psychiatric Institute. Unipolar patients with an early onset disease have a greater familial morbidity for depression, alcoholism and sociopathy than unipolar patients with a late onset disease. There is an excess of unipolar depression in female relatives of early onset unipolars when compared to late onset probands, regardless of the proband's sex. Alcoholism and sociopathy are also more prevalent in the relatives of early onset unipolars versus late onset probands. Our morbidity risk data show familial genetic differences between early and late onset forms of unipolar illness and partially confirm Winokur's concept of two subtypes of unipolar depression.


1972 ◽  
Vol 120 (556) ◽  
pp. 265-266 ◽  
Author(s):  
George Winokur

A major problem in the affective disorders is what constitutes an homogeneous illness. A recent study enabled us to separate depressive illnesses into two types (1). The first we have called ‘depression spectrum disease’; its prototype is a female with an onset of a depressive illness before the age of 40, in whose family more depression is seen in female relatives than in male relatives, the deficit in males being made up by alcoholism and sociopathy. The second illness we have called ‘pure depressive disease’, the prototype of which is a male whose depression starts after age 40 and in whom there are equal amounts of depression in both male and female relatives and no large amount of alcoholism or sociopathy in the males. First degree relatives of depression spectrum disease are more likely to be psychiatrically ill (depression, sociopathy or alcoholism) than first degree relatives of pure depressive disease probands. Data of Hopkinson and Ley support this concept in part (2); they found that early-onset affective probands (< 40) had higher morbid risks for affective illness in relatives than late-onset probands (onset after 40). Further confirmation comes from a study of 259 alcoholics and their first degree relatives (3). Most of the psychiatrically ill male relatives had alcoholism; most of the psychiatrically ill female relatives had depression. As of the present the differentiation of the two kinds of depressive illness is made on the basis of a specific familial predisposition. Major clinical differences in the two groups have eluded us.


US Neurology ◽  
2010 ◽  
Vol 06 (01) ◽  
pp. 41
Author(s):  
Roy N Alcalay ◽  
Cheryl Waters ◽  
◽  

Early-onset Parkinson’s disease (EOPD) is defined as disease onset before 40 or 50 years of age. The clinical characteristics of EOPD are very similar to those of late-onset PD, but dystonia is more often a presenting symptom, dementia is rare, and disease progression may be slower. Mutations in several genes have been described in cases with EOPD, often with strong family history, including mutations in α-synuclein (SNCA),DJ-1, PTEN-induced kinase-1 (PINK-1), andATP13A2. However, the most common mutations identified in EOPD are in Parkin (PRKN), leucine-rich repeat kinase 2 (LRRK2), and glucocerebrosidase (GBA). With the exception ofSNCAandATP13A2carriers, mutation carriers are often indistinguishable from non-carriers. Large series of EOPD cases that are not ascertained by family history estimate mutation frequency at 4–16%. Given that the frequency of positive family history is much higher, we believe that many genetic risk factors are yet to be discovered.


1975 ◽  
Vol 127 (1) ◽  
pp. 75-77 ◽  
Author(s):  
George Winokur ◽  
Remi Cadoret ◽  
M. Baker ◽  
J. Dorzab

In a recent letter to this Journal, Galdi (1974) stated, ‘Through what is … a genetic approach to classification, Winokur and associates … reported the isolation of two subtypes of unipolar depressive disorder differentiated by age of onset and contrasting family history pattern.’ These subtypes (Winokur, 1974) are termed depression spectrum disease (early-onset; most likely female; familial alcoholism and/or antisocial personality) and pure depressive disease (late onset; equally male or female; little familial alcoholism and/or antisocial personality).


1995 ◽  
Vol 167 (5) ◽  
pp. 649-652 ◽  
Author(s):  
R. C. Baldwin ◽  
Barbara Tomenson

BackgroundDepression in later life is often thought to differ from that at other times of adulthood. The evidence for this is controversial but is important to any proposed organic model of depression in the elderly. Here, early- and late-onset depressions in later life are compared.MethodFifty-seven depressed patients with a mean age of 74 were studied, 21 with an early onset (aged 59 or less) and 36 with a late onset. All were suffering from major depression according to DSM–III–R. The measures at entry included severity and symptoms, cognitive function, antecedent life events, physical health and vascular risk factors and/or vascular disease. We also recorded any family history of mood disorders, as well as the course of illness.ResultsThe anxiety item scores of the Hamilton Depression Rating Scale were significantly higher in those with an early onset, but otherwise symptoms differed little. Heritability was greater in the early-onset group. There was a striking association of vascular disease and/or risk with late-onset patients.ConclusionsVascular disease is associated with late-onset depression. This is consistent with the hypothesis that depression in later life is a more ‘biological’ disorder.


1998 ◽  
Vol 10 (1) ◽  
pp. 3-6
Author(s):  
Clive Holmes

Following on from the hypothesis of a role for the ApoE ε4 and ε2 alleles as risk and protective factors, respectively, for late-onset Alzheimer's disease (AD) came inevitable questions regarding other psychiatric conditions of late onset including depressive illness and schizophrenia. Is ApoE ε4 a risk factor in these diseases and do carriers have an earlier age of onset? Does ApoE ε2 have a protective role, with carriers of this allele having a later age of onset?


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