Home - Australian Pharmacist

The mythic mint

Dr Leigh Dayton - 10 November 2022

Bottle of essential oil with fresh mint leaves, illustrating mythic mint benefits

Clinical

From candy canes and tasty teas to digestive disorders and sniffly sinuses – this herb is a sweet treat that may help boost health. Attracted...

Are pop-ups doing more harm than good?

Ruth Cooper - 27 June 2025

Industry

Are decision-support tools the problem or the cure for patient safety? Australian Pharmacist investigates.

What the Aged Care Royal Commission means for pharmacists

Mikaela Dery - 6 February 2019

Industry

When the Aged Care Royal Commission began in February, Minister for Aged Care Ken Wyatt, released a statement reaffirming the government’s commitment to the regulation...

Opinion: Withdraw all homeopathic products – now!

Dr Iqbal Ramzan - 26 November 2019

Opinion

With no evidence of efficacy why are pharmacists still selling homeopathy products? The position of the PSA on Homeopathy is to be commended. In the...

2022 is a year of action for PSA

Jennifer Cooke - 9 February 2022

Industry

Ahead of a federal election and an energised remuneration campaign, PSA‘s Communities of Specialty Interest are preparing to power pharmacy practice in 2022 and beyond.

Breast cancer awareness more important than ever

Chloe Hava - 27 October 2021

Industry

This Breast Cancer Awareness month, pharmacists should urge women to remain vigilant about screening after months of lockdown for many.

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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

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?

What’s on the list?

Making palliative care support easier to find

Supporting patients and families at the end of life

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

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?

What’s on the list?

Making palliative care support easier to find

Supporting patients and families at the end of life

Case scenario

Introduction