What is Tacrine?

Introduction

Tacrine is a centrally acting acetylcholinesterase inhibitor and indirect cholinergic agonist (parasympathomimetic).

It was the first centrally acting cholinesterase inhibitor approved for the treatment of Alzheimer’s disease, and was marketed under the trade name Cognex. Tacrine was first synthesised by Adrien Albert at the University of Sydney in 1949. It also acts as a histamine N-methyltransferase inhibitor.

Clinical Use

Tacrine was the prototypical cholinesterase inhibitor for the treatment of Alzheimer’s disease. William K. Summers received a patent for this use in 1989. Studies found that it may have a small beneficial effect on cognition and other clinical measures, though study data was limited and the clinical relevance of these findings was unclear.

Tacrine has been discontinued in the US in 2013, due to concerns over safety.

Tacrine was also described as an analeptic agent used to promote mental alertness.

Adverse Effects

  • Very common (>10% incidence) adverse effects include:
    • Increased LFTs.
    • Nausea.
    • Vomiting.
    • Diarrhoea.
    • Headache.
    • Dizziness.
  • Common (1-10% incidence) adverse effects include:
    • Indigestion.
    • Belching.
    • Abdominal pain.
    • Myalgia – muscle pain.
    • Confusion.
    • Ataxia – decreased control over bodily movements.
    • Insomnia.
    • Rhinitis.
    • Rash.
    • Fatigue.
    • Weight loss.
    • Constipation.
    • Somnolence.
    • Tremor.
    • Anxiety.
    • Urinary incontinence.
    • Hallucinations.
    • Agitation.
    • Conjunctivitis (a link to tacrine treatment has not been conclusively proven).
    • Diaphoresis – sweating.
  • Uncommon/rare (<1% incidence) adverse effects include:
    • Hepatotoxicity (that is toxic effects on the liver).
    • Ototoxicity (hearing/ear damage; a link to tacrine treatment has not been conclusively proven).
    • Seizures.
    • Agranulocytosis (a link between treatment and this adverse effect has not been proven) – a potentially fatal drop in white blood cells, the body’s immune/defensive cells.
    • Taste changes.
  • Unknown incidence adverse effects include:
    • Urinary tract infection.
    • Delirium.
    • Other optic effects such as glaucoma, cataracts, etc. (also not conclusively linked to tacrine treatment).
    • Depression.
    • Suicidal ideation and behaviour.
    • Hypotension.
    • Bradycardia.

Overdose

As stated above, overdosage of tacrine may give rise to severe side effects such as nausea, vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Atropine is a popular treatment for overdose.

Pharmacokinetics

Major form of metabolism is in the liver via hydroxylation of benzylic carbon by CYP1A2. This forms the major metabolite 1-hydroxy-tacrine (velnacrine) which is still active.

On This Day … 14 June

People (Births)

  • 1864 – Alois Alzheimer, German psychiatrist and neuropathologist (d. 1915).

Alois Alzheimer

Alois Alzheimer (14 June 1864 to 19 December 1915) was a German psychiatrist and neuropathologist and a colleague of Emil Kraepelin. Alzheimer is credited with identifying the first published case of “presenile dementia”, which Kraepelin would later identify as Alzheimer’s disease.

After graduating from Wurzburg as a Doctor of Medicine in 1887, he spent five months assisting mentally ill women before he took an office in the city mental asylum in Frankfurt, the Städtische Anstalt für Irre und Epileptische (Asylum for Lunatics and Epileptics). Emil Sioli, a noted psychiatrist, was the dean of the asylum. Another neurologist, Franz Nissl, began to work in the same asylum with Alzheimer. Together, they conducted research on the pathology of the nervous system, specifically the normal and pathological anatomy of the cerebral cortex. Alzheimer was the co-founder and co-publisher of the journal Zeitschrift für die gesamte Neurologie und Psychiatrie, though he never wrote a book that he could call his own.

While at the Frankfurt asylum, Alzheimer also met Emil Kraepelin, one of the best-known German psychiatrists of the time. Kraepelin became a mentor to Alzheimer, and the two worked very closely for the next several years. When Kraepelin moved to Munich to work at the Royal Psychiatric Hospital in 1903, he invited Alzheimer to join him.

At the time, Kraepelin was doing clinical research on psychosis in senile patients; Alzheimer, on the other hand, was more interested in the lab work of senile illnesses. The two men would face many challenges involving the politics of the psychiatric community. For example, both formal and informal arrangements would be made among psychiatrists at asylums and universities to receive cadavers.

In 1904, Alzheimer completed his Habilitation at Ludwig Maximilian University of Munich, where he was appointed as a professor in 1908. Afterwards, he left Munich for the Silesian Friedrich Wilhelm University in Breslau in 1912, where he accepted a post as professor of psychiatry and director of the Neurologic and Psychiatric Institute. His health deteriorated shortly after his arrival so that he was hospitalised. Alzheimer died three years later.

Auguste Deter

In 1901, Alzheimer observed a patient at the Frankfurt asylum named Auguste Deter. The 51-year-old patient had strange behavioral symptoms, including a loss of short-term memory; she became his obsession over the coming years. Auguste Deter was a victim of the politics of the time in the psychiatric community; the Frankfurt asylum was too expensive for her husband. Herr Deter made several requests to have his wife moved to a less expensive facility, but Alzheimer intervened in these requests. Frau Deter, as she was known, remained at the Frankfurt asylum, where Alzheimer had made a deal to receive her records and brain upon her death.

On 8 April 1906, Frau Deter died, and Alzheimer had her medical records and brain brought to Munich where he was working in Kraepelin’s laboratory. With two Italian physicians, he used the staining techniques of Bielschowsky to identify amyloid plaques and neurofibrillary tangles. These brain anomalies would become identifiers of what later became known as Alzheimer’s disease.

Another hypothesis offered by Claire O’Brien was that Auguste Deter actually had a vascular dementing disease.

Findings

Alzheimer discussed his findings on the brain pathology and symptoms of presenile dementia publicly on 03 November 1906, at the Tübingen meeting of the Southwest German Psychiatrists. The attendees at this lecture seemed uninterested in what he had to say. The lecturer that followed Alzheimer was to speak on the topic of “compulsive masturbation”, which the audience was so eagerly awaiting that they sent Alzheimer away without any questions or comments on his discovery of the pathology of a type of senile dementia.

Following the lecture, Alzheimer published a short paper summarizing his lecture; in 1907 he wrote a larger paper detailing the disease and his findings. The disease would not become known as Alzheimer’s disease until 1910, when Kraepelin named it so in the chapter on “Presenile and Senile Dementia” in the 8th edition of his Handbook of Psychiatry. By 1911, his description of the disease was being used by European physicians to diagnose patients in the US.

Contemporaries

American Solomon Carter Fuller gave a report similar to that of Alzheimer at a lecture five months before Alzheimer. Oskar Fischer was a fellow German psychiatrist, 12 years Alzheimer’s junior, who reported 12 cases of senile dementia in 1907 around the time that Alzheimer published his short paper summarizing his lecture.

Alzheimer and Fischer had different interpretations of the disease, but due to Alzheimer’s short life, they never had the opportunity to meet and discuss their ideas.

Among the doctors trained by Alois Alzheimer and Emil Kraepelin at München in the beginning of the XXth century were the Spanish neuropathologists Nicolás Achúcarro and Gonzalo Rodríguez Lafora, two distinguished disciples of Santiago Ramón y Cajal and members of the Spanish Neurological School. Alzheimer recommended the young and brilliant Nicolás Achúcarro to organise the neuropathological service at the Government Hospital for the Insane, at Washington D.C. (current, NIH), and after two years of work, he was substituted by Gonzalo Rodríguez Lafora.

Other Interests

Alzheimer was known for having a variety of medical interests including vascular diseases of the brain, early dementia, brain tumours, forensic psychiatry and epilepsy. Alzheimer was a leading specialist in histopathology in Europe. His colleagues knew him to be a dedicated professor and cigar smoker.

Linking Putative Blood Somatic Mutations, Alzheimer’s & PTSD

Research Paper Title

Putative Blood Somatic Mutations in Post-Traumatic Stress Disorder-Symptomatic Soldiers: High Impact of Cytoskeletal and Inflammatory Proteins.

Background

The recently discovered autism/intellectual disability somatic mutations in postmortem brains, presenting higher frequency in Alzheimer’s disease subjects, compared with the controls. They further revealed high impact cytoskeletal gene mutations, coupled with potential cytoskeleton-targeted repair mechanisms.

The current study was aimed at further discerning if somatic mutations in brain diseases are presented only in the most affected tissue (the brain), or if blood samples phenocopy the brain, toward potential diagnostics.

Methods

Variant calling analyses on an RNA-seq database including peripheral blood samples from 85 soldiers (58 controls and 27 with symptoms of post-traumatic stress disorder, PTSD) was performed.

Results

High (e.g. protein truncating) as well as moderate impact (e.g., single amino acid change) germline and putative somatic mutations in thousands of genes were found. Further crossing the mutated genes with autism, intellectual disability, cytoskeleton, inflammation, and DNA repair databases, identified the highest number of cytoskeletal-mutated genes (187 high and 442 moderate impact). Most of the mutated genes were shared and only when crossed with the inflammation database, more putative high impact mutated genes specific to the PTSD-symptom cohorts versus the controls (14 versus 13) were revealed, highlighting tumour necrosis factor specifically in the PTSD-symptom cohorts.

Conclusions

With microtubules and neuro-immune interactions playing essential roles in brain neuroprotection and Alzheimer-related neurodegeneration, the current mutation discoveries contribute to mechanistic understanding of PTSD and brain protection, as well as provide future diagnostics toward personalised military deployment strategies and drug design.

Reference

Sragovich, S., Gershovits, M., Lam, J.C.K., Li, V.O.K. & Gozes, I. (2021) Putative Blood Somatic Mutations in Post-Traumatic Stress Disorder-Symptomatic Soldiers: High Impact of Cytoskeletal and Inflammatory Proteins. Journal of Alzheimer’s Disease. doi: 10.3233/JAD-201158. Online ahead of print.

On This Day … 19 December

People (Births)

  • 1925 – William Schutz, American psychologist and academic (d. 2002).

People (Deaths)

  • 1915 – Alois Alzheimer, German psychiatrist and neuropathologist (b. 1864).

William Schultz

William Schutz (19 December 1925 to 09 November 2002) was an American psychologist.

Biography

Schutz was born in Chicago, Illinois. He practiced at the Esalen Institute in the 1960s. He later became the president of BConWSA International. He received his PhD from UCLA. In the 1950s, he was part of the peer-group at the University of Chicago’s Counselling Centre that included Carl Rogers, Thomas Gordon, Abraham Maslow and Elias Porter. He taught at Tufts University, Harvard University, University of California, Berkeley and the Albert Einstein College of Medicine, and was chairman of the holistic studies department at Antioch University until 1983.

In 1958, Schutz introduced a theory of interpersonal relations he called Fundamental Interpersonal Relations Orientation (FIRO). According to the theory three dimensions of interpersonal relations were deemed to be necessary and sufficient to explain most human interaction: Inclusion, Control and Affection. These dimensions have been used to assess group dynamics.

Schutz also created FIRO-B, a measurement instrument with scales that assess the behavioural aspects of the three dimensions. His advancement of FIRO Theory beyond the FIRO-B tool was most obvious in the change of the “Affection” scale to the “Openness” scale in the “FIRO Element-B”. This change highlighted his newer theory that behaviour comes from feelings (“FIRO Element-F”) and the self-concept (“FIRO Element-S”). “Underlying the behaviour of openness is the feeling of being likable or unlikeable, lovable or unlovable. I find you likable if I like myself in your presence, if you create an atmosphere within which I like myself.”

W. Schutz authored more than ten books and many articles. His work was influenced by Alexander Lowen, Ida Pauline Rolf and Moshe Feldenkrais. As a body therapist he led encounter group workshops focussing on the underlying causes of illnesses and developing alternative body-centred cures. His books, “Profound Simplicity” and “The Truth Option,” address this theme. He brought new approaches to body therapy that integrated truth, choice (freedom), (self) responsibility, self-esteem, self-regard and honesty into his approach.

In his books one encounters the concept of energy cycles (e.g. Schutz 1979) which a person goes through or call for completion. The single steps of the energy cycles are: motivation – prepare – act – feel.

Schutz died at his home in Muir Beach, California in 2002.

Influences

While teaching and doing research at Harvard, the University of Chicago, the University of California at Berkeley, and other institutions, Schutz focused on psychology but also studied philosophy – in particular, the scientific method, the philosophy of science, logical empiricism, and research design (with both Hans Reichenbach and Abraham Kaplan). He also worked with Paul Lazarsfeld, the well-known sociologist and methodologist and Elvin Semrad, professor of psychiatry at Harvard Medical School and clinical director in charge of psychiatric residency training at the Massachusetts Mental Health Centre. For Schutz, Semrad was a key figure, “a brilliant, earthy psychoanalyst who became my main mentor about groups.”

An avid student, Schutz also learned T-group methodology (“T” for training) at the National Training Laboratories (NTL) at Bethel, Maine, psychosynthesis, a spiritually oriented technique involving imagery, devised by an Italian contemporary of Freud named Roberto Assagioli, psychodrama with Hannah Weiner, bioenergetics with Alexander Lowen and John Pierrakos, Rolfing with Ida Rolf, and Gestalt Therapy with Paul Goodman. In his own words, “I tried everything physical, psychological, and spiritual – all diets, all therapies, all body methods, jogging, meditating, visiting a guru in India, and fasting for thirty-four days on water. These experiences counterbalanced my twenty years in science and left me with a strong desire to integrate the scientific with the experiential.”

Alois Alzheimer

Aloysius Alzheimer (also known as Alois Alzheimer; 14 June 1864 to 19 December 1915) was a German psychiatrist and neuropathologist and a colleague of Emil Kraepelin. Alzheimer is credited with identifying the first published case of “presenile dementia”, which Kraepelin would later identify as Alzheimer’s disease.

Early Life and Education

Aloysius Alzheimer was born in Marktbreit, Bavaria on 14 June 1864, the son of Anna Johanna Barbara Sabina and Eduard Román Alzheimer. His father served in the office of notary public in the family’s hometown.

The Alzheimers moved to Aschaffenburg when Alois was still young in order to give their children an opportunity to attend the Royal Humanistic Gymnasium. After graduating with Abitur in 1883, Alzheimer studied medicine at University of Berlin, University of Tübingen, and University of Würzburg. In his final year at university, he was a member of a fencing fraternity, and even received a fine for disturbing the peace while out with his team. In 1887, Alois Alzheimer graduated from Würzburg as Doctor of Medicine.

Career

The following year, he spent five months assisting mentally ill women before he took an office in the city mental asylum in Frankfurt am Main, the Städtische Anstalt für Irre und Epileptische (Asylum for Lunatics and Epileptics). Emil Sioli, a noted psychiatrist, was the dean of the asylum. Another neurologist, Franz Nissl, began to work in the same asylum with Alzheimer. Together, they conducted research on the pathology of the nervous system, specifically the normal and pathological anatomy of the cerebral cortex. Alzheimer was the co-founder and co-publisher of the journal Zeitschrift für die gesamte Neurologie und Psychiatrie, though he never wrote a book that he could call his own.

While at the Frankfurt asylum, Alzheimer also met Emil Kraepelin, one of the best-known German psychiatrists of the time. Kraepelin became a mentor to Alzheimer, and the two worked very closely for the next several years. When Kraepelin moved to Munich to work at the Royal Psychiatric Hospital in 1903, he invited Alzheimer to join him.

At the time, Kraepelin was doing clinical research on psychosis in senile patients; Alzheimer, on the other hand, was more interested in the lab work of senile illnesses. The two men would face many challenges involving the politics of the psychiatric community. For example, both formal and informal arrangements would be made among psychiatrists at asylums and universities to receive cadavers.

In 1904, Alzheimer completed his Habilitation at Ludwig Maximilian University of Munich, where he was appointed as a professor in 1908. Afterwards, he left Munich for the Silesian Friedrich Wilhelm University in Breslau in 1912, where he accepted a post as professor of psychiatry and director of the Neurologic and Psychiatric Institute. His health deteriorated shortly after his arrival so that he was hospitalized. Alzheimer died three years later.

Auguste Deter

In 1901, Alzheimer observed a patient at the Frankfurt asylum named Auguste Deter. The 51-year-old patient had strange behavioural symptoms, including a loss of short-term memory; she became his obsession over the coming years. Auguste Deter was a victim of the politics of the time in the psychiatric community; the Frankfurt asylum was too expensive for her husband. Herr Deter made several requests to have his wife moved to a less expensive facility, but Alzheimer intervened in these requests. Frau Deter remained at the Frankfurt asylum, where Alzheimer had made a deal to receive her records and brain upon her death.

On 08 April 1906, Frau Deter died, and Alzheimer had her medical records and brain brought to Munich where he was working in Kraepelin’s laboratory. With two Italian physicians, he used the staining techniques of Bielschowsky to identify amyloid plaques and neurofibrillary tangles. These brain anomalies would become identifiers of what later became known as Alzheimer’s disease.

Another hypothesis offered by Claire O’Brien was that Auguste Deter actually had a vascular dementing disease.

Findings

Alzheimer discussed his findings on the brain pathology and symptoms of presenile dementia publicly on 03 November 1906, at the Tübingen meeting of the Southwest German Psychiatrists. The attendees at this lecture seemed uninterested in what he had to say. The lecturer that followed Alzheimer was to speak on the topic of “compulsive masturbation”, which the audience was so eagerly awaiting that they sent Alzheimer away without any questions or comments on his discovery of the pathology of a type of senile dementia.

Following the lecture, Alzheimer published a short paper summarising his lecture; in 1907 he wrote a larger paper detailing the disease and his findings. The disease would not become known as Alzheimer’s disease until 1910, when Kraepelin named it so in the chapter on “Presenile and Senile Dementia” in the 8th edition of his Handbook of Psychiatry. By 1911, his description of the disease was being used by European physicians to diagnose patients in the US.

Contemporaries

American Solomon Carter Fuller gave a report similar to that of Alzheimer at a lecture five months before Alzheimer. Oskar Fischer was a fellow German psychiatrist, 12 years Alzheimer’s junior, who reported 12 cases of senile dementia in 1907 around the time that Alzheimer published his short paper summarizing his lecture.

Alzheimer and Fischer had different interpretations of the disease, but due to Alzheimer’s short life, they never had the opportunity to meet and discuss their ideas.

Among the doctors trained by Alois Alzheimer and Emil Kraepelin at München in the beginning of the XXth century were the Spanish neuropathologists Nicolás Achúcarro and Gonzalo Rodríguez Lafora, two distinguished disciples of Santiago Ramón y Cajal and members of the Spanish Neurological School. Alzheimer recommended the young and brilliant Nicolás Achúcarro to organize the neuropathological service at the Government Hospital for the Insane, at Washington D.C. (current, NIH), and after two years of work, he was substituted by Gonzalo Rodríguez Lafora.

Other Interests

Alzheimer was known for having a variety of medical interests including vascular diseases of the brain, early dementia, brain tumours, forensic psychiatry and epilepsy. Alzheimer was a leading specialist in histopathology in Europe. His colleagues knew him to be a dedicated professor and cigar smoker.

Death

In August 1912, Alzheimer fell ill on the train on his way to the University of Breslau, where he had been appointed professor of psychiatry in July 1912. Most probably he had a streptococcal infection and subsequent rheumatic fever leading to valvular heart disease, heart failure and kidney failure. He had not recovered completely from this illness.

He died of heart failure on 19 December 1915 at age 51, in Breslau, Silesia (present-day Wrocław, Poland). He was buried on 23 December 1915 next to his wife in the Hauptfriedhof in Frankfurt am Main.

Depression and Pre-Clinical Dementia

Research Paper Title

A cross-national study of depression in preclinical dementia: A COSMIC collaboration study.

Background

Depression commonly accompanies Alzheimer’s disease, but the nature of this association remains uncertain.

Methods

Longitudinal data from the COSMIC consortium were harmonized for eight population-based cohorts from four continents. Incident dementia was diagnosed in 646 participants, with a median follow-up time of 5.6 years to diagnosis. The association between years to dementia diagnosis and successive depressive states was assessed using a mixed effect logistic regression model. A generic inverse variance method was used to group study results, construct forest plots, and generate heterogeneity statistics.

Results

A common trajectory was observed showing an increase in the incidence of depression as the time to dementia diagnosis decreased despite cross-national variability in depression rates.

Conclusions

The results support the hypothesis that depression occurring in the preclinical phases of dementia is more likely to be attributable to dementia-related brain changes than environment or reverse causality.

Reference

Carles, S., Carriere, I., Reppermund, S., Davin, A., Guaita, A., Vaccaro, R., Ganguli, M., Jacobsen, E.P., Beer, J.C., Riedel-Heller, S.G., Roehr, S., Pabst, A., Haan, M.N., Brodarty, H., Kochan, N.A., Trollor, J.N., Kim, K.W., Han, J.W., Suh, S.W., Lobo, A., De La Camara, C., Lobo, E., Lipnicki, D.M., Sachdev, P.S., Ancelin, M-L., Ritchie, K. & for Cohrot Studies of Memory in an International Consortium (COSMIC). (2020) A cross-national study of depression in preclinical dementia: A COSMIC collaboration study. Alzheimer’s & Dementia. doi: 10.1002/alz.12149. Online ahead of print.

Alzheimer’s Disease: Carers and their Mental Health

Research Paper Title

Predictors of mental health problems in formal and informal caregivers of patients with Alzheimer’s disease.

Background

Caring for a person with Alzheimer’s disease (AD) is associated with significant mental burden e.g., depression and anxiety, and difficulties with social, familial, and professional functioning. To date, few studies have examined variables which would allow for a comprehensive and detailed study of the relationship between personal resources and caregiver health status, with a majority of studies focusing on factors that contribute to increased caregiver’s burden. Moreover, the available evidence fails to address differences in the functioning of formal and informal carers. Paying proper attention to the problems of nursing home staff can help identify important risk factors. Therefore, this study compared mental health problems in informal and formal caregivers and examined the relationship between mental resources and mental health problems in both groups of caregivers.

Methods

This cross-sectional study examined 100 formal (n = 50) and informal (n = 50) caregivers of AD patients. Personal resources were measured with the Social Support Questionnaire (SSQ), the Generalised Self-Efficacy Scale (GSES), and the Sense of Coherence Questionnaire (SCQ), while mental health was assessed with the Depression Assessment Questionnaire (DAQ) and the General Health Questionnaire (GHQ). Multivariate stepwise regression was performed separately for both investigated groups.

Results

There were no significant differences between informal and formal caregivers in terms of psychological variables, i.e., sense of coherence, social support, self-efficacy, or mental health problems. In contrast, there were different significant predictors of mental health problems in both groups. Comprehensibility (SCQ) was a significant predictor of mental health problems measured by DAQ and self-efficacy (GSES) was a significant predictor of mental health problems measured by GHQ in informal caregivers. For formal caregivers, emotional support (SSQ) and comprehensibility (SCQ) were significant predictors of mental health problems measured by DAQ, while tangible support (SSQ) and meaningfulness (SCQ) were significant predictors of mental health problems measured by GHQ.

Conclusions

Personal resources are significant predictors of mental health outcomes in caregivers of AD patients. Preventive actions should therefore include assessment of factors affecting caregivers’ mental health in order to provide them with necessary care and create appropriate support groups.

Reference

Soltys, A. & Tyburski, E. (2020) Predictors of mental health problems in formal and informal caregivers of patients with Alzheimer’s disease. BMC Psychiatry. 20(1), pp.435. doi: 10.1186/s12888-020-02822-7.

Is Type 2 Diabetes an Independent Risk Factor for Alzheimer Patients with Depression?

Research Paper Title

Analysis of Risk Factors for Depression in Alzheimer’s Disease Patients.

Background

Depression, which affects about 52% of Alzheimer’s disease (AD) patients, can worsen cognitive impairment and increase mortality and suicide rates.

The researchers hope to provide clinical evidence for the prevention and treatment of depression in AD patients by investigating related risk factors of depression in AD patients.

Methods

158 AD inpatients of the Department of Neurology, Daping Hospital from September 2017 to March 2019 were enrolled. General information, laboratory tests, cognitive and emotional function assessments of the inpatients were collected.

Logistic regression was used to analyse the risk factors of depression in AD patients, and the relationship between 17 Hamilton depression scale scores and HbA1c levels in AD patients was further analysed.

Results

The prevalence of age, gender, hypertension, hyperlipidemia, Type 2 diabetes mellitus (T2DM), and white matter lesions (WML) in the AD with depression group was significantly different from without depression group.

Hypertension, T2DM, and WML are independent risk factors for depression in AD patients.

The depression scores of AD patients with HbA1c>6.5% were significantly higher than AD patients with HbA1c ≤ 6.5%, and there were significant difference in depression scale scores between using anti-diabetes drugs group and not using anti-diabetes drugs group whose HbA1c level is >6.5%, while no difference in depression scores between using anti-diabetes drugs group and not using anti-diabetes drugs group whose HbA1c level is ≤6.5%.

Conclusions

T2DM is an independent risk factor for AD patients with depression.

Increased HbA1c levels aggravate depression in AD patients, and controlling HbA1c levels and anti-diabetes drugs can reduce the severity of depression in AD patients.

Reference

Yang, H., Hong, W., Chen, L., Tao, Y., Peng, Z. & Zhou, H. (2020) Analysis of Risk Factors for Depression in Alzheimer’s Disease Patients. The International Journal of Neuroscience. 1-6. doi: 10.1080/00207454.2020.1730369. Online ahead of print.