Epidemiology of Dementias and Alzheimer’s Disease

Sosa‐Ortíz, Ana Luisa; Acosta‐Castillo, Gilberto Isaac; Prince, Martin

doi:10.1016/j.arcmed.2012.11.003

Cited by 440 publications

(273 citation statements)

References 66 publications

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“…Although rates of chronic conditions in this group were high for both TMBs and CMBs, many chronic conditions that typically occur or worsen in older ages were observed to be even more common among TMBs. [26][27][28][29][30][31][32][33] In this study, we observed that TMBs had higher rates of hypertension, congestive heart failure, coronary artery disease, hyperlipidemia, arthritis, dementia, stroke, Chronic Kidney Disease, and diabetes, compared to their CMB counterparts. The literature on the burden of these types of nonmental health chronic conditions in transgender individuals is very sparse, especially in the United States, and even more so for older transgender adults.…”

Section: Trans Medicare Beneficiaries and Chronic Conditions 407 Discusmentioning

confidence: 75%

Transgender Medicare Beneficiaries and Chronic Conditions: Exploring Fee-for-Service Claims Data

et al. 2017

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Purpose: Data on the health and well-being of the transgender population are limited. However, using claims data we can identify transgender Medicare beneficiaries (TMBs) with high confidence. We seek to describe the TMB population and provide comparisons of chronic disease burden between TMBs and cisgender Medicare beneficiaries (CMBs), thus laying a foundation for national level TMB health disparity research. Methods: Using a previously validated claims algorithm based on ICD-9-CM codes relating to transsexualism and gender identity disorder, we identified a cohort of TMBs using Medicare Fee-for-Service (FFS) claims data. We then describe the demographic characteristics and chronic disease burden of TMBs (N = 7454) and CMBs (N = 39,136,229). Results: Compared to CMBs, a greater observed proportion of TMBs are young (under age 65) and Black, although these differences vary by entitlement. Regardless of entitlement, TMBs have more chronic conditions than CMBs, and more TMBs have been diagnosed with asthma, autism spectrum disorder, chronic obstructive pulmonary disease, depression, hepatitis, HIV, schizophrenia, and substance use disorders. TMBs also have higher observed rates of potentially disabling mental health and neurological/chronic pain conditions, as well as obesity and other liver conditions (nonhepatitis), compared to CMBs. Conclusion: This is the first systematic look at chronic disease burden in the transgender population using Medicare FFS claims data. We found that TMBs experience multiple chronic conditions at higher rates than CMBs, regardless of Medicare entitlement. TMBs under age 65 show an already heavy chronic disease burden which will only be exacerbated with age.

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Section: Trans Medicare Beneficiaries and Chronic Conditions 407 Discusmentioning

confidence: 75%

Transgender Medicare Beneficiaries and Chronic Conditions: Exploring Fee-for-Service Claims Data

et al. 2017

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“…Dementia is caused by many different disorders, resulting in deterioration of memory, mental functions, and behavior. It was estimated that, globally, in 2010, 35.6 million people were living with it-and it was predicted that this number would double every year: Alzheimer's disease (AD) is generally considered to be the most common subtype, resulting in 60-80% of cases [186]. As it is associated with the e x c e s s i v e b u i l d -u p o f β -a m y l o i d ( A β ) and hyperphosphorylated forms of the microtubuleassociated protein, tau, this led to the proposal of the Bamyloid cascade hypothesis^as the underlying pathogenic basis for this disease [187].…”

Section: Neurodegenerative Diseasesmentioning

confidence: 99%

Molecular Targets of Cannabidiol in Neurological Disorders

Bih

Chen

Nunn³

et al. 2015

Neurotherapeutics

462

323

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Cannabis has a long history of anecdotal medicinal use and limited licensed medicinal use. Until recently, alleged clinical effects from anecdotal reports and the use of licensed cannabinoid medicines are most likely mediated by tetrahydrocannabinol by virtue of: 1) this cannabinoid being present in the most significant quantities in these preparations; and b) the proportion:potency relationship between tetrahydrocannabinol and other plant cannabinoids derived from cannabis. However, there has recently been considerable interest in the therapeutic potential for the plant cannabinoid, cannabidiol (CBD), in neurological disorders but the current evidence suggests that CBD does not directly interact with the endocannabinoid system except in vitro at supraphysiological concentrations. Thus, as further evidence for CBD's beneficial effects in neurological disease emerges, there remains an urgent need to establish the molecular targets through which it exerts its therapeutic effects. Here, we conducted a systematic search of the extant literature for original articles describing the molecular pharmacology of CBD. We critically appraised the results for the validity of the molecular targets proposed. Thereafter, we considered whether the molecular targets of CBD identified hold therapeutic potential in relevant neurological diseases. The molecular targets identified include numerous classical ion channels, receptors, transporters, and enzymes. Some CBD effects at these targets in in vitro assays only manifest at high concentrations, which may be difficult to achieve in vivo, particularly given CBD's relatively poor bioavailability. Moreover, several targets were asserted through experimental designs that demonstrate only correlation with a given target rather than a causal proof. When the molecular targets of CBD that were physiologically plausible were considered for their potential for exploitation in neurological therapeutics, the results were variable. In some cases, the targets identified had little or no established link to the diseases considered. In others, molecular targets of CBD were entirely consistent with those already actively exploited in relevant, clinically used, neurological treatments. Finally, CBD was found to act upon a number of targets that are linked to neurological therapeutics but that its actions were not consistent withmodulation of such targets that would derive a therapeutically beneficial outcome. Overall, we find that while >65 discrete molecular targets have been reported in the literature for CBD, a relatively limited number represent plausible targets for the drug's action in neurological disorders when judged by the criteria we set. We conclude that CBD is very unlikely to exert effects in neurological diseases through modulation of the endocannabinoid system. Moreover, a number of other molecular targets of CBD reported in the literature are unlikely to be of relevance owing to effects only being observed at supraphysiological concentrations. Of interest and after excludin...

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“…Currently, more than 35 million people are suffering from AD, and this figure is projected to grow to 106.8 million people by 2050 [2] . Apart from the slow and progressive degeneration process with synaptic loss leading to a final neuronal death, the accumulation of amyloid β (Aβ) plaques and the formation of neurofibrillary tangles (NFTs) in the brain are accepted as the main hallmarks of AD [3] .…”

Section: Introductionmentioning

confidence: 99%

LX2343 alleviates cognitive impairments in AD model rats by inhibiting oxidative stress-induced neuronal apoptosis and tauopathy

et al. 2017

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alzheimer's disease (aD) is a progressive neurodegenerative disease leading to the irreversible loss of brain neurons and cognitive abilities, and the vicious interplay between oxidative stress (OS) and tauopathy is believed to be one of the major players in aD development. Here, we demonstrated the capability of the small molecule N-(1,3-benzodioxol-5-yl)-2-[5-chloro-2-methoxy(phenylsulfonyl)anilino]acetamide (LX2343) to ameliorate the cognitive dysfunction of aD model rats by inhibiting OS-induced neuronal apoptosis and tauopathy. Streptozotocin (STZ) was used to induce OS in neuronal cells in vitro and in aD model rats that were made by intracerebroventricular injection of STZ (3 mg/kg, bilaterally), and Morris water maze test was used to evaluate the cognitive dysfunction in ICV-STZ rats. Treatment with LX2343 (5-20 μmol/L) significantly attenuated STZ-induced apoptosis in SH-SY5Y cells and mouse primary cortical neurons by alleviating OS and inhibiting the JNK/p38 and pro-apoptotic pathways. LX2343 was able to restore the integrity of mitochondrial function and morphology, increase aTP biosynthesis, and reduce ROS accumulation in the neuronal cells. In addition, LX2343 was found to be a non-ATP competitive GSK-3β inhibitor with IC 50 of 1.84±0.07 μmol/L, and it potently inhibited tau hyperphosphorylation in the neuronal cells. In ICV-STZ rats, administration of LX2343 (7, 21 mg·kg -1 ·d -1 , ip, for 5 weeks) efficiently improved their cognitive deficits. LX2343 ameliorates the cognitive dysfunction in the AD model rats by suppressing OS-induced neuronal apoptosis and tauopathy, thus highlighting the potential of LX2343 for the treatment of aD.

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Epidemiology of Dementias and Alzheimer’s Disease

Cited by 440 publications

References 66 publications

Transgender Medicare Beneficiaries and Chronic Conditions: Exploring Fee-for-Service Claims Data

Transgender Medicare Beneficiaries and Chronic Conditions: Exploring Fee-for-Service Claims Data

Molecular Targets of Cannabidiol in Neurological Disorders

LX2343 alleviates cognitive impairments in AD model rats by inhibiting oxidative stress-induced neuronal apoptosis and tauopathy

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