Affective symptoms and AT(N) biomarkers in mild cognitive impairment and Alzheimer’s disease: A systematic literature review

Banning, Leonie C.P.; Ramakers, Inez H.G.B.; Deckers, Kay; Verhey, Frans R.J.; Aalten, Pauline

doi:10.1016/j.neubiorev.2019.09.014

Cited by 39 publications

(41 citation statements)

References 70 publications

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“…According to a recent systematic review, the association between CSF AD biomarkers and depression and apathy in mild cognitive impairment (MCI) and AD dementia has been examined in 16 and 3 studies, respectively. 9 Overall, no evidence was found that associated depression with amyloid, p-tau or t-tau. The authors hypothesized that this null-finding could be due to the grouping of heterogeneous phenotypes together.…”

Section: Introductionmentioning

confidence: 98%

Alzheimer's disease biomarkers as predictors of trajectories of depression and apathy in cognitively normal individuals, mild cognitive impairment, and Alzheimer's disease dementia

Banning

Ramakers

Rosenberg

et al. 2020

Int J Geriat Psychiatry

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Objectives: To examine trajectories of depression and apathy over a 5-year followup period in (prodromal) Alzheimer's disease (AD), and to relate these trajectories to AD biomarkers. Methods: The trajectories of depression and apathy (measured with the Neuropsychiatric Inventory or its questionnaire) were separately modeled using growth mixture models for two cohorts (National Alzheimer's Coordinating Center, NACC, n = 22 760 and Alzheimer's Disease Neuroimaging Initiative, ADNI, n = 1 733). The trajectories in ADNI were associated with baseline CSF AD biomarkers (Aβ 42, t-tau, and p-tau) using bias-corrected multinomial logistic regression. Results: Multiple classes were identified, with the largest classes having no symptoms over time. Lower Aβ 42 and higher tau (ie, more AD pathology) was associated with increased probability of depression and apathy over time, compared to classes without symptoms. Lower Aβ 42 (but not tau) was associated with a steep increase of apathy, whereas higher tau (but not Aβ 42) was associated with a steep decrease of apathy.

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Section: Introductionmentioning

confidence: 98%

Alzheimer's disease biomarkers as predictors of trajectories of depression and apathy in cognitively normal individuals, mild cognitive impairment, and Alzheimer's disease dementia

Banning

Ramakers

Rosenberg

et al. 2020

Int J Geriat Psychiatry

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“…Neurodegenerative diseases of the nervous system are always related to impaired learning and memory ability, eventually inducing to cognitive disorders [1]. AD is the leading cause of cognitive deficits and the most common neurodegenerative disease of aging [2].…”

Section: Introductionmentioning

confidence: 99%

Lemon essential oil ameliorates age-associated cognitive dysfunction via modulating hippocampal synaptic density and inhibiting acetylcholinesterase

Liu

Kou

et al. 2020

Aging

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The lemon essential oil (LEO), extracted from the fruit of lemon, has been used to treat multiple pathological diseases, such as diabetes, inflammation, cardiovascular diseases, depression and hepatobiliary dysfunction. The study was designed to study the effects of LEO on cognitive dysfunction induced by Alzheimer's disease (AD). We used APP/PS1 double transgene (APP/PS1) AD mice in the experiment; these mice exhibit significant deficits in synaptic density and hippocampal-dependent spatial related memory. The effects of LEO on learning and memory were examined using the Morris Water Maze (MWM) test, Novel object recognition test, and correlative indicators, including a neurotransmitter (acetylcholinesterase, AChE), a nerve growth factor (brainderived neurotrophic factor, BDNF), a postsynaptic marker (PSD95), and presynaptic markers (synapsin-1, and synaptophysin), in APP/PS1 mice. Histopathology was performed to estimate the effects of LEO on AD mice. A significantly lowered brain AChE depression in APP/PS1 and wild-type C57BL/6L (WT) mice. PSD95/ Synaptophysin, the index of synaptic density, was noticeably improved in histopathologic changes. Hence, it can be summarized that memory-enhancing activity might be associated with a reduction in the AChE levels and is elevated by BDNF, PSD95, and synaptophysin through enhancing synaptic plasticity.

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“…APP, MAPT, APOE, and other variants in pathogenic genes (Table 1) as well as the presence of schizophrenia-and/or depression-related SNPs [25][26][27], together with additional metabolic disorders [28], cerebrovascular risk or consolidated vascular damage [4,[29][30][31], premorbid personality [32], and inappropriate management may contribute to BDs in AD. BDs partially correlate with conventional biomarkers of dementia [33,34]; however, agitation/aggression correlates with AD cerebrospinal fluid (CSF) biomarkers, and depression is inversely associated with core AD CSF pathology (low Aβ42, high Tau, and high pTau) [35,36]. Over 50% of AD patients show comorbidities (TDP-43 and Lewy bodies) which associate with frontotemporal lobar degeneration and LBD.…”

Section: Introductionmentioning

confidence: 99%

Pharmacogenomics of Cognitive Dysfunction and Neuropsychiatric Disorders in Dementia

Cacabelos

2020

IJMS

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Symptomatic interventions for patients with dementia involve anti-dementia drugs to improve cognition, psychotropic drugs for the treatment of behavioral disorders (BDs), and different categories of drugs for concomitant disorders. Demented patients may take >6–10 drugs/day with the consequent risk for drug–drug interactions and adverse drug reactions (ADRs >80%) which accelerate cognitive decline. The pharmacoepigenetic machinery is integrated by pathogenic, mechanistic, metabolic, transporter, and pleiotropic genes redundantly and promiscuously regulated by epigenetic mechanisms. CYP2D6, CYP2C9, CYP2C19, and CYP3A4/5 geno-phenotypes are involved in the metabolism of over 90% of drugs currently used in patients with dementia, and only 20% of the population is an extensive metabolizer for this tetragenic cluster. ADRs associated with anti-dementia drugs, antipsychotics, antidepressants, anxiolytics, hypnotics, sedatives, and antiepileptic drugs can be minimized by means of pharmacogenetic screening prior to treatment. These drugs are substrates, inhibitors, or inducers of 58, 37, and 42 enzyme/protein gene products, respectively, and are transported by 40 different protein transporters. APOE is the reference gene in most pharmacogenetic studies. APOE-3 carriers are the best responders and APOE-4 carriers are the worst responders; likewise, CYP2D6-normal metabolizers are the best responders and CYP2D6-poor metabolizers are the worst responders. The incorporation of pharmacogenomic strategies for a personalized treatment in dementia is an effective option to optimize limited therapeutic resources and to reduce unwanted side-effects.

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Affective symptoms and AT(N) biomarkers in mild cognitive impairment and Alzheimer’s disease: A systematic literature review

Cited by 39 publications

References 70 publications

Alzheimer's disease biomarkers as predictors of trajectories of depression and apathy in cognitively normal individuals, mild cognitive impairment, and Alzheimer's disease dementia

Alzheimer's disease biomarkers as predictors of trajectories of depression and apathy in cognitively normal individuals, mild cognitive impairment, and Alzheimer's disease dementia

Lemon essential oil ameliorates age-associated cognitive dysfunction via modulating hippocampal synaptic density and inhibiting acetylcholinesterase

Pharmacogenomics of Cognitive Dysfunction and Neuropsychiatric Disorders in Dementia

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