Increased Hippocampal Plaques and Tangles in Patients With Alzheimer Disease With a Lifetime History of Major Depression

Rapp, Michael A.; Schnaider‐Beeri, Michal; Grossman, Hillel; Sano, Mary; Perl, Daniel P.; Purohit, Dushyant P.; Gorman, Jack M.; Haroutunian, Vahram

doi:10.1001/archpsyc.63.2.161

Cited by 341 publications

(250 citation statements)

References 50 publications

Supporting

Mentioning

221

Contrasting

Unclassified

Order By: Relevance

“…A separate prospective study, which conducted a neuropathological evaluation of the post-mortem brains of patients with a mean age of 81 years, found the presence of a higher number of neuritic plaques and neurofibrillary tangle formations in the hippocampus of patients with AD with a history of depression, as compared with brains of AD patients without depression history (Rapp et al 2006).…”

Section: Bipolar Disorder and Depressionmentioning

confidence: 99%

Alzheimer´s Disease associated with Psychiatric Comorbidities

Garcez

Falchetti

Mina

et al. 2015

An. Acad. Bras. Ciênc.

View full text Add to dashboard Cite

Alzheimer's disease (AD) is the most common cause of dementia and has become a severe public health issue. It is estimated that globally, 35.6% of people have some form of dementia. This number is expected to double by 2030, and possibly even triple by 2050. The disease is associated with deficits in cognition/ memory and a reduced ability in coping with everyday life. Moreover, patients can experience behavioral alterations such as mood swings, depression and hallucinations. Therefore, it is common to find the presence of neuropsychiatric comorbidities such as depression, schizophrenia and bipolar disorder during the course or development of AD. These disorders can become severe enough to interfere with the patients daily functioning, and can worsen the course of the disease. However, little is known about the causal relationship between psychiatric comorbidities and AD, or the reasons for the predisposition of some individuals to such disorders. Therefore, the purpose of this review is to clarify the causal relationship between depression, schizophrenia and bipolar disorder with AD.

show abstract

Section: Bipolar Disorder and Depressionmentioning

confidence: 99%

Alzheimer´s Disease associated with Psychiatric Comorbidities

Garcez

Falchetti

Mina

et al. 2015

An. Acad. Bras. Ciênc.

View full text Add to dashboard Cite

show abstract

“…There is evidence that hippocampal atrophy, in addition to being a classic feature of many dementias and aging itself, confers vulnerability to depression. 47-48 Some of the processes with presumed etiological roles could be subsumed under the vascular or inflammatory hypotheses, but others such as amyloid plaque formation 49-50 are unique to this hypothesis. Interestingly, hippocampal regions have been found to be especially vulnerable to ischemia 51 and to activation of the hypothalamic-pituitary-adrenal (HPA) axis, resulting from stress and chronic medical illness.…”

Section: Current Hypotheses For Biological Mechanisms Promoting Lldmentioning

confidence: 99%

The Age-by-Disease Interaction Hypothesis of Late-Life Depression

McKinney

Sibille

2013

The American Journal of Geriatric Psychiatry

View full text Add to dashboard Cite

The phenomenological diagnosis of depression is successful in increasing diagnostic reliability, but it is a classification scheme without biological bases. One subtype of depression for which evidence suggests a unique biological basis is late-life depression (LLD), with first onset of symptoms after the age of 65. LLD is common and poses a significant burden on affected individuals, caretakers, and society. The pathophysiology of LLD includes disruptions of the neural network underlying mood, which can be conceptualized as the result of dysfunction in multiple underlying biological processes. Here, we briefly review current LLD hypotheses and then describe the characteristics of molecular brain aging and their overlap with disease processes. Further, we propose a new hypothesis for LLD, the Age-by-Disease Interaction hypothesis, which posits that the clinical presentation of LLD is the integrated output of specific biological processes that are pushed in LLD-promoting directions by changes in gene expression naturally occurring during brain aging, hence leading the brain to a physiological state that is more susceptible to LLD, since additional pushes by genetic, environmental and biochemical factors may now be sufficient to generate dysfunctional states that produce depressive symptoms. We put our propositions together into a decanalization model to aid in illustrating how age-related biological changes of the brain can shift the repertoire of available functional states in a pro-depression direction, and how additional factors can readily lead the system into distinct and stable maladaptive phenotypes, including LLD. This model brings together basic research on neuropsychiatric and neurodegenerative diseases more closely with the investigation of normal aging. Specifically, identifying biological processes affected during normal aging may inform the development of new interventions for the prevention and treatment of LLD.

show abstract

“…Three patients with AD pathology also displayed evidence of vascular disease and the other three demonstrated Lewy body pathology (dementia with Lewy bodies being the secondary diagnosis). In another recent neuropathological study, increased numbers of plaques and tangles in the hippocampal region were identified in post mortem tissue in AD patients with prior episodes of major depression (Rapp et al, 2006). The density of plaques and tangles were even greater in patients in whom there was concurrent depression and dementia at the time of the initial AD diagnosis (Rapp et al, 2006).…”

Section: The Role Of Amyloid and Taumentioning

confidence: 96%

“…MDD has been identified both as a risk factor and a prodrome of Alzheimer's disease (AD) in clinical and community samples (Reding et al, 1985;Kral and Emery, 1989;Kokmen et al, 1991;Jorm et al, 1991;Alexopoulos et al, 1993b;Speck et al, 1995;Devanand et al, 1996;Henderson et al, 1997;Steffens et al, 1997;Bassuk et al, 1998;Chen et al, 1999;Yaffe et al, 1999;Geerlings et al, 2000;Jorm, 2000;Lockwood et al, 2000;Visser et al, 2000;Jorm, 2001;Lockwood et al, 2002;Wilson et al, 2002;Green et al, 2003;Sweet et al, 2004;Cannon-Spoor et al, 2005;Gatz et al, 2006;Rapp et al, 2006;Steffens et al, 2006). Community based studies have identified clinical depression, including depressive symptoms as a risk factor for the subsequent development of dementia.…”

Section: Relationship Of Mdd To Admentioning

confidence: 99%