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Anxiety, apathy and depression are common in subjects with mild cognitive impairment (MCI) and may herald Alzheimer's disease (AD). We investigated whether these symptoms correlated with cerebrospinal fluid (CSF) markers for AD in subjects with MCI.
Subjects with MCI (n=268) were selected from the ‘Development of screening guidelines and criteria for pre-dementia Alzheimer's disease’ (DESCRIPA) and Alzheimer's Disease Neuroimaging Initiative (ADNI) studies. We measured amyloid β(1-42) protein (Aβ42) and total tau (t-tau) in CSF. Neuropsychiatric symptoms were measured with the Neuropsychiatric Inventory.
Depressive symptoms were reported by 55 subjects (21%), anxiety by 35 subjects (13%) and apathy by 49 subjects (18%). The presence of anxiety was associated with abnormal CSF Aβ42 [odds ratio (OR) 2.3, 95% confidence interval (CI) 1.6–3.3] and t-tau (OR 2.6, 95% CI 1.9–3.6) concentrations and with the combination of abnormal concentrations of both Aβ42 and t-tau (OR 3.1, 95% CI 2.0–4.7). The presence of agitation and irritability was associated with abnormal concentrations of Aβ42 (agitation: OR 1.6, 95% CI 1.1–2.3; irritability: OR 2.2, 95% CI 1.5–3.3). Symptoms of depression and apathy were not related to any of the CSF markers.
In subjects with MCI, symptoms of anxiety, agitation and irritability may reflect underlying AD pathology, whereas symptoms of depression and apathy do not.
Schizophrenia is a human specific disease, unknown in other primates. Low adiposity during childhood was associated with a greater risk of developing schizophrenia, but this disease has a higher incidence in the obese children and adults, too.
We developed a new hypothesis on the human evolution. According to it, changes in the activity of the IGF1 (insulin-like growth factor1)/insulin pathway (altered in human pathological conditions such as the psychiatric disorders) could be responsible for the appearance of certain specific human traits.
This hypothesis predicts that schizophrenia should result from a deviation of the normal IGF1/insulin signaling in brain in both directions. A drug that increases insulin resistance should improve the condition in the slim patients and worsen them in the obese patients.
A multi-center double-blind study on palmitate paliperidone (pp), the major active metabolite of the antipsychotic risperidone (that increases insulin resistance and stimulates weight gain), was conducted. 25–150 mg eq pp was injected intramuscular (into the deltoid muscle or the gluteal muscle) at 1 week interval for 1 year in a double blind study in patients with acute symptoms.
Our preliminary observations based on the Positive and Negative Syndrome Scale (PANSS) total scores showed that the slim patients had statistically the best response to pp and the worse effects were observed in the obese patients. The study is still ongoing.
These results suggest that schizophrenia is a polarized disease with 2 major phenotypes- one with either insulin sensitivity or obesity and insulin resistance.
Alzheimer disease (AD) is one of the most common neurodegenerative disorders (prevalence boosts from 0.2% in patients aged 55-65 up to 27% in patients aged 85+ years. Clinical manifestations of psychiatric disorders accompanying hypo- and hyper-thyroid function can mimic cognitive impairment.
Our study aimed at studying the relationship between thyroid pathology, anxiety disorder and Alzheimer disease (AD).
Our longitudinal, prospective research followed 49 patients with thyroid disorders (aged 50-85 years, 93.5 females); 63.3% (n = 31) had coexisting dementia and thyroid disease while 36.7% (n = 18) were dementia-cleared (10 had mild cognitive impairment (MCI) and 8 - anxiety and/or depression); we cross/analyzed control (n = 18) and target (n = 31) groups.
In the target group, 64.5% (n = 20) had hypothyroidism, 22.6% (n = 7) had euthyroid function and 12.9% (n = 4) had hyperthyroidism. The prevalence of anxiety and depression was higher in the hypothyroidism + dementia group (55.5%, n = 11) than in the hypothyroidism-only group (44.4%, n = 8). Most controls (77.8%, n = 14) had hypothyroidism while 22% (n = 4) had normal thyroid function.
Anxiety disorder had a greater prevalence both in the group with dementia + thyroid disease and in the MCI group. Hypothyroidism was the dominant thyroid disorder in both groups. The early diagnostic and treatment of thyroid disease is expected to improve prognosis and evolution of future cognitive disorders (MCI & AD).
Estimates for Romanian patients with dementia range from 200,000 to 300,000, but reports warn that actual numbers may be higher.
Based on our experience we inferred that specific personality changes may occur in patients with mild cognitive impairment (MCI) and Alzheimer (AD).
We tried to quantify such personality changes in MCI and AD patients.
We designed an observational study (n = 60 patients, aged 55+) with MCI (n = 30; 50% male; mean age ∼ 73) and moderate AD (n = 30; 43.3% male (n = 13); mean age ∼74). We “profiled” patient personality (Woodworth - Mathews questionnaire) and identified the most prominent features.
The most prominent feature in MCI was depression (80%, n = 24) followed by impulsive (26.7%, n = 8) and emotional (23.3%, n = 7) tendencies. Moderate AD patients exhibited less depression (43%, n = 13). Twice more AD patients exhibited paranoid tendencies (36.7%, n = 11) as compared to MCI patients (16.7%, n = 5); schizoid tendencies in moderate AD reached 23.3% (n = 7) vs. 0.03% (n = 1) in MCI patients. Hypochondria, obsessions, emotional instability and antisocial behavior were similar.
Different dominant personality features as noted in MCI (depressive, impulsive and emotional tendencies) and moderate AD (paranoid, schizoid tendencies) require personalized treatment. Some features (depressive, impulsive and emotional tendencies) tend to be accentuated in MCI (barely impaired self awareness). Aggravated paranoid or schizoid tendencies in AD may result from impaired awareness; however, altered control over previously “dormant” personality features should be considered.
Diagnosing Alzheimer Disease (AD) is a long-lasting process, mainly due to the variability of initial symptoms (i.e. memory problems, speech difficulties, behavioral changes). Patients are usually either unaware of their difficulties or attempting to conceal them.
We wanted to establish whether, based on existing knowledge, a better understanding of the leading causes of miscommunication can overcome communication barriers for AD patients.
We tried to summarize the existing recommendations and gold-practices and to contract them into key messages in order to improve quality of communication.
We performed a systematic overview of medical literature (PubMed search, disclos* OR communic* NOT communicate AND Alzheimer), selecting of the 516 resulting titles those papers focused on doctor/patient and doctor/caregiver communication issues.
Specific communication requirements were identified for effective collaboration between
(1) physician and patient,
(2) physician and patient's caregivers/family and
(3) caregivers/family and patient.
A minimal set of communication skills and predictable courses of action was further developed, depending on
(a) best practices and
(b) recommended practices.
Although communicating with people with Alzheimer is difficult, quite often the communication barriers are mainly due to an inaccurate perception of the disease and of patient limitations and disabilities. Understanding the mechanisms involved and acquiring certain interpersonal habits may significantly improve communication effectiveness, particularly in mild and moderate AD.
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