Home - Australian Pharmacist

Coronavirus: Australia ‘alert but not alarmed’

AP Staff - 22 January 2020

Industry

‘Precautionary and active surveillance’ is required to manage the risk of a novel coronavirus outbreak in China, Australia’s Chief Medical Officer Professor Brendan Murphy...

What collaborative prescribing could look like for pharmacists

James Chalmers - 28 July 2019

Industry

PSA CEO Dr Shane Jackson has backed the likelihood of pharmacists being able to prescribe under a collaborative framework by the end of next...

The long road to remunerated consultations

Warren Blee FPS - 1 October 2022

Industry

Like the great plague of 1665, the COVID-19 pandemic has demonstrated the value of pharmacists, and accelerated practice evolution.

A breast cancer drug for seizures

Dr Esther Lau - 7 August 2017

Clinical

Status epilepticus is a medical emergency. It is commonly defined as 30 minutes of continuous seizure activity, or repeated seizures without full recovery of...

Why you can’t miss PSA21

Ruth Cooper - 21 July 2021

Industry

With a diverse program of clinical, therapeutic and industry sessions for pharmacists in all practice settings, PSA21 will help grow your medicines expertise.

Rural healthcare advocate honoured

Peter Guthrey FPS - 28 January 2025

People

NSW pharmacist Anna Barwick MPS was awarded the Medal of the Order of Australia (OAM) in the 2025 Australia Day Honours.

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Causes of dementia	Descriptions
Alzheimer’s disease	The amyloid cascade hypothesis suggests that the deposition of amyloid-β (Aβ) plaques leads to neurofibrillary tangles, cell loss, vascular damage and dementia.3 For decades, this hypothesis has been the primary target for developing therapies for Alzheimer’s disease. In light of new evidence, several iterations of the theory have been proposed, highlighting a more complex aetiology involving polygenic, epigenetic, environmental, vascular, neuroinflammatory and metabolic factors.4 Today, the aetiological complexity surrounding the pathogenesis of Alzheimer’s disease has not been fully established.
Vascular dementia	Vascular dementia results from impaired blood supply to the brain, which damages brain tissue and subsequently leads to cognitive decline.5 Common neuropathological findings include multiple infarcts or single strategic infarcts caused by atherothromboembolic events or small vessel disease.5
Mixed dementia	It is common for individuals to present with more than one type of dementia. The term ‘mixed dementia’ refers to the co-occurrence of more than one subtype of dementia, most commonly Alzheimer’s disease and vascular dementia. However, the use of this term is increasingly discouraged due to its ambiguity.6
Lewy body dementia	Lewy body dementia is an umbrella term describing two forms of dementia: dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD). DLB is characterised by the accumulation of α-synuclein in Lewy bodies and Lewy neurites in the brain, as well as neuronal loss in the substantia nigra, although typically less severe than that observed in Parkinson’s disease.6 PDD and DLB are both α-synucleinopathies.6 There is considerable clinical overlap between DLB and PDD.6 Generally, DLB presents at an older age, while PDD is preceded by a long period of motor symptoms.6 The arbitrary ‘1-year rule’ is commonly applied in clinical practice, whereby DLB is diagnosed when cognitive symptoms appear before or within 1 year of motor symptoms, whereas PDD is diagnosed when cognitive decline occurs in the context of established Parkinson’s disease.6
Frontotemporal dementia	Frontotemporal dementia (FTD) is a common cause of early-onset dementia, typically affecting individuals aged 45–65 years.7 FTD is categorised as three variants: 1) behavioural-variant FTD (associated with behavioural and executive deficits), 2) non-fluent variant primary progressive aphasia (progressive deficits in speech, grammar and word output), and 3) semantic-variant primary progressive aphasia (impaired naming and single-word comprehension).8 As the name suggests, FTD involves progressive degeneration of the frontal and/or temporal lobes associated with characteristic protein inclusions.6 Genetic mutations and family history of dementia play an important role in its pathogenesis.6
Other causes of dementia	Other less common causes of dementia are associated with9,10: Huntington’s disease traumatic brain injury posterior cortical atrophy infectious disease (e.g. human immunodeficiency virus [HIV], Creutzfeldt-Jakob disease) toxicity (e.g. hazardous alcohol consumption).

Causes of dementia	Descriptions
Alzheimer’s disease	The amyloid cascade hypothesis suggests that the deposition of amyloid-β (Aβ) plaques leads to neurofibrillary tangles, cell loss, vascular damage and dementia.3 For decades, this hypothesis has been the primary target for developing therapies for Alzheimer’s disease. In light of new evidence, several iterations of the theory have been proposed, highlighting a more complex aetiology involving polygenic, epigenetic, environmental, vascular, neuroinflammatory and metabolic factors.4 Today, the aetiological complexity surrounding the pathogenesis of Alzheimer’s disease has not been fully established.
Vascular dementia	Vascular dementia results from impaired blood supply to the brain, which damages brain tissue and subsequently leads to cognitive decline.5 Common neuropathological findings include multiple infarcts or single strategic infarcts caused by atherothromboembolic events or small vessel disease.5
Mixed dementia	It is common for individuals to present with more than one type of dementia. The term ‘mixed dementia’ refers to the co-occurrence of more than one subtype of dementia, most commonly Alzheimer’s disease and vascular dementia. However, the use of this term is increasingly discouraged due to its ambiguity.6
Lewy body dementia	Lewy body dementia is an umbrella term describing two forms of dementia: dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD). DLB is characterised by the accumulation of α-synuclein in Lewy bodies and Lewy neurites in the brain, as well as neuronal loss in the substantia nigra, although typically less severe than that observed in Parkinson’s disease.6 PDD and DLB are both α-synucleinopathies.6 There is considerable clinical overlap between DLB and PDD.6 Generally, DLB presents at an older age, while PDD is preceded by a long period of motor symptoms.6 The arbitrary ‘1-year rule’ is commonly applied in clinical practice, whereby DLB is diagnosed when cognitive symptoms appear before or within 1 year of motor symptoms, whereas PDD is diagnosed when cognitive decline occurs in the context of established Parkinson’s disease.6
Frontotemporal dementia	Frontotemporal dementia (FTD) is a common cause of early-onset dementia, typically affecting individuals aged 45–65 years.7 FTD is categorised as three variants: 1) behavioural-variant FTD (associated with behavioural and executive deficits), 2) non-fluent variant primary progressive aphasia (progressive deficits in speech, grammar and word output), and 3) semantic-variant primary progressive aphasia (impaired naming and single-word comprehension).8 As the name suggests, FTD involves progressive degeneration of the frontal and/or temporal lobes associated with characteristic protein inclusions.6 Genetic mutations and family history of dementia play an important role in its pathogenesis.6
Other causes of dementia	Other less common causes of dementia are associated with9,10: Huntington’s disease traumatic brain injury posterior cortical atrophy infectious disease (e.g. human immunodeficiency virus [HIV], Creutzfeldt-Jakob disease) toxicity (e.g. hazardous alcohol consumption).

Causes of dementia	Descriptions
Alzheimer’s disease	The amyloid cascade hypothesis suggests that the deposition of amyloid-β (Aβ) plaques leads to neurofibrillary tangles, cell loss, vascular damage and dementia.3 For decades, this hypothesis has been the primary target for developing therapies for Alzheimer’s disease. In light of new evidence, several iterations of the theory have been proposed, highlighting a more complex aetiology involving polygenic, epigenetic, environmental, vascular, neuroinflammatory and metabolic factors.4 Today, the aetiological complexity surrounding the pathogenesis of Alzheimer’s disease has not been fully established.
Vascular dementia	Vascular dementia results from impaired blood supply to the brain, which damages brain tissue and subsequently leads to cognitive decline.5 Common neuropathological findings include multiple infarcts or single strategic infarcts caused by atherothromboembolic events or small vessel disease.5
Mixed dementia	It is common for individuals to present with more than one type of dementia. The term ‘mixed dementia’ refers to the co-occurrence of more than one subtype of dementia, most commonly Alzheimer’s disease and vascular dementia. However, the use of this term is increasingly discouraged due to its ambiguity.6
Lewy body dementia	Lewy body dementia is an umbrella term describing two forms of dementia: dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD). DLB is characterised by the accumulation of α-synuclein in Lewy bodies and Lewy neurites in the brain, as well as neuronal loss in the substantia nigra, although typically less severe than that observed in Parkinson’s disease.6 PDD and DLB are both α-synucleinopathies.6 There is considerable clinical overlap between DLB and PDD.6 Generally, DLB presents at an older age, while PDD is preceded by a long period of motor symptoms.6 The arbitrary ‘1-year rule’ is commonly applied in clinical practice, whereby DLB is diagnosed when cognitive symptoms appear before or within 1 year of motor symptoms, whereas PDD is diagnosed when cognitive decline occurs in the context of established Parkinson’s disease.6
Frontotemporal dementia	Frontotemporal dementia (FTD) is a common cause of early-onset dementia, typically affecting individuals aged 45–65 years.7 FTD is categorised as three variants: 1) behavioural-variant FTD (associated with behavioural and executive deficits), 2) non-fluent variant primary progressive aphasia (progressive deficits in speech, grammar and word output), and 3) semantic-variant primary progressive aphasia (impaired naming and single-word comprehension).8 As the name suggests, FTD involves progressive degeneration of the frontal and/or temporal lobes associated with characteristic protein inclusions.6 Genetic mutations and family history of dementia play an important role in its pathogenesis.6
Other causes of dementia	Other less common causes of dementia are associated with9,10: Huntington’s disease traumatic brain injury posterior cortical atrophy infectious disease (e.g. human immunodeficiency virus [HIV], Creutzfeldt-Jakob disease) toxicity (e.g. hazardous alcohol consumption).

Causes of dementia	Descriptions
Alzheimer’s disease	The amyloid cascade hypothesis suggests that the deposition of amyloid-β (Aβ) plaques leads to neurofibrillary tangles, cell loss, vascular damage and dementia.3 For decades, this hypothesis has been the primary target for developing therapies for Alzheimer’s disease. In light of new evidence, several iterations of the theory have been proposed, highlighting a more complex aetiology involving polygenic, epigenetic, environmental, vascular, neuroinflammatory and metabolic factors.4 Today, the aetiological complexity surrounding the pathogenesis of Alzheimer’s disease has not been fully established.
Vascular dementia	Vascular dementia results from impaired blood supply to the brain, which damages brain tissue and subsequently leads to cognitive decline.5 Common neuropathological findings include multiple infarcts or single strategic infarcts caused by atherothromboembolic events or small vessel disease.5
Mixed dementia	It is common for individuals to present with more than one type of dementia. The term ‘mixed dementia’ refers to the co-occurrence of more than one subtype of dementia, most commonly Alzheimer’s disease and vascular dementia. However, the use of this term is increasingly discouraged due to its ambiguity.6
Lewy body dementia	Lewy body dementia is an umbrella term describing two forms of dementia: dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD). DLB is characterised by the accumulation of α-synuclein in Lewy bodies and Lewy neurites in the brain, as well as neuronal loss in the substantia nigra, although typically less severe than that observed in Parkinson’s disease.6 PDD and DLB are both α-synucleinopathies.6 There is considerable clinical overlap between DLB and PDD.6 Generally, DLB presents at an older age, while PDD is preceded by a long period of motor symptoms.6 The arbitrary ‘1-year rule’ is commonly applied in clinical practice, whereby DLB is diagnosed when cognitive symptoms appear before or within 1 year of motor symptoms, whereas PDD is diagnosed when cognitive decline occurs in the context of established Parkinson’s disease.6
Frontotemporal dementia	Frontotemporal dementia (FTD) is a common cause of early-onset dementia, typically affecting individuals aged 45–65 years.7 FTD is categorised as three variants: 1) behavioural-variant FTD (associated with behavioural and executive deficits), 2) non-fluent variant primary progressive aphasia (progressive deficits in speech, grammar and word output), and 3) semantic-variant primary progressive aphasia (impaired naming and single-word comprehension).8 As the name suggests, FTD involves progressive degeneration of the frontal and/or temporal lobes associated with characteristic protein inclusions.6 Genetic mutations and family history of dementia play an important role in its pathogenesis.6
Other causes of dementia	Other less common causes of dementia are associated with9,10: Huntington’s disease traumatic brain injury posterior cortical atrophy infectious disease (e.g. human immunodeficiency virus [HIV], Creutzfeldt-Jakob disease) toxicity (e.g. hazardous alcohol consumption).

Case scenario

Introduction

Learning outcomes

Pathophysiology

Box 1 – Common symptoms of dementia

Differential diagnosis

Diagnosis

Risk factors

Management

Non-pharmacological treatment

Pharmacological treatment

Additional support

Knowledge to practice

Conclusion

Case scenario continued

Key points

Our authors

References

Day one: clinical insights and celebrating talent

Day two: expanding scope and emerging technologies

Day three: practical insights and professional reflection

1. Diphtheria is back

2. Vaccination rates keep declining

3. Pharmacist's busiest flu-vaccine week on record!

4. HPV vaccination success

5. Maternal and infant RSV vaccination rates have already improved

6. What does the future hold for vaccination?

Practical guidance

Box 1: Practical advice for communicating with autistic patients

Box 2: Using AAC to support communication

Case 1

Case 2

Box 3: Tips for conducting HMRs with autistic patients

1. Who is now funded under the NIP?

2. Which RSV vaccine is funded for older Australians?

3. When does the NIP listing commence?

4. Will booster doses be required?

5. What was the reason behind the decision?

6. What does ATAGI have to say?

Case scenario

Introduction

Learning outcomes

Pathophysiology

Box 1 – Common symptoms of dementia

Differential diagnosis

Diagnosis

Risk factors

Management

Non-pharmacological treatment

Pharmacological treatment

Additional support

Knowledge to practice

Conclusion

Case scenario continued

Key points

Our authors

References

Day one: clinical insights and celebrating talent

Day two: expanding scope and emerging technologies

Day three: practical insights and professional reflection

1. Diphtheria is back

2. Vaccination rates keep declining

3. Pharmacist's busiest flu-vaccine week on record!

4. HPV vaccination success

5. Maternal and infant RSV vaccination rates have already improved

6. What does the future hold for vaccination?

Practical guidance

Box 1: Practical advice for communicating with autistic patients

Box 2: Using AAC to support communication

Case 1

Case 2

Box 3: Tips for conducting HMRs with autistic patients

1. Who is now funded under the NIP?

2. Which RSV vaccine is funded for older Australians?

3. When does the NIP listing commence?

4. Will booster doses be required?

5. What was the reason behind the decision?

6. What does ATAGI have to say?

Case scenario

Introduction