What is Alzheimer’s Disease

Alzheimer’s disease stands as a formidable foe in the realm of neurodegenerative conditions, impacting millions globally. It’s a name that often conjures images of memory loss and cognitive decline, but the reality of Alzheimer’s encompasses far more than these well-known symptoms. It’s a complex, multifaceted disease that weaves a web of challenges for both those living with it and their caregivers.

At its core, Alzheimer’s is marked by its neurodegenerative nature – a gradual, relentless breakdown of neurons, eroding the very fabric of memory and cognitive function. These last two points being the hallmark of dementia.

But the story doesn’t end there.

Accompanying the cognitive deficits is a constellation of neuropsychiatric symptoms. These include mood disturbances like depression, episodes of agitation, and bouts of irritability, each adding layers of complexity to the condition.

The impact of these symptoms extends beyond the individual; they deeply affect the quality of life of caregivers and family members, painting a picture of a disease that is not just a personal battle but a communal challenge.

Understanding Alzheimer’s disease, therefore, is not just about grasping its cognitive aspects but also about appreciating the broader, more nuanced picture of its impact on the human experience.

Neuropsychiatric Symptoms in Alzheimer’s

In the landscape of Alzheimer’s disease and related dementias, one of the most prevalent and challenging aspects is the array of behavioural and psychological symptoms that accompany these conditions. Known collectively as neuropsychiatric symptoms (NPSs), sadly, they’re not mere footnotes in the narrative of dementia; they play a starring role in the lives of over 80% of those affected.

These NPSs encompass a range of manifestations – from irritability and night time disturbances to more overt agitation. Their impact is profound and far-reaching, influencing not just the patients themselves but the entire ecosystem of care around them. They are linked to an array of stark outcomes:

• higher mortality rates,
• more frequent hospitalisations,
• earlier need for institutional care, and a significant dip in the quality of life.
• For caregivers, these symptoms often translate into heightened distress and, on a broader scale, escalate healthcare costs.

Yet, despite the clear clinical footprint of these NPSs, their underpinnings remain somewhat enigmatic. Their neurobiological origins are like pieces of a complex puzzle that we’re still piecing together. This is the crux of ongoing research and studies – to delve deeper into the brain’s workings in Alzheimer’s and unravel the mysteries of these neuropsychiatric symptoms.

That’s where this new study comes in.

Recognising the impact of neuropsychiatric symptoms on both individuals with Alzheimer’s and their caregivers is crucial. It’s far more than academic; it’s a key that could unlock better management strategies, alleviate the burden on patients and caregivers, and ultimately improve the quality of life for those ensnared in the grip of these challenging conditions.

At OT Brisbane, we understand the challenges faced by caregivers in navigating these changes. That’s where evidence-based programs like the Tailored Activity Program come into play, offering practical solutions at home which are in line with the observations made in this study.

But first, here’s a little background on neuroinflammation, the brain and Alzheimer’s. 

Neuroinflammation’s role in the brain is a tale of complexity and duality. It’s a response mechanism within the central nervous system (CNS), essentially the brain’s way of sounding an alarm in the face of threats – be they from infection, traumatic injury, toxic substances, metabolic mishaps, or autoimmune disorders. Think of it as the brain’s immune system kicking into high gear.

This is where things get intricate.

The process begins with a trigger, akin to the first domino in a chain reaction, leading to the activation of the brain’s own immune cells, notably microglial cells and astrocytes. These cells then release a barrage of inflammatory mediators

• pro-inflammatory cytokines, chemokines, and reactive oxygen species.

It’s a bit like an emergency response team rushing to a crisis; however, in their zeal to protect, they can inadvertently cause collateral damage kicking off a snowballs roll of progressive chronic inflammation.

This damage manifests in various ways in the human brain. At a cellular level, the inflammatory molecules can directly harm brain cells, compromising their functionality. The effects ripple outward, impacting overall brain function.

The symptoms aren’t just abstract biological phenomena; they translate into tangible cognitive declines, age-related impairments, loss of quality of life, loss of independence and a predisposition to an array of neurological diseases, including heavy hitters like Alzheimer’s, Parkinson’s disease, multiple sclerosis, and the consequences of stroke.

So, while neuroinflammation starts as a protective mechanism, its prolonged or misdirected action can become deleterious.

It’s a fine line between defence and damage. Understanding this balance – knowing when and how to modulate this inflammatory response – is a key puzzle piece in managing and potentially preventing the progression of numerous neurodegenerative conditions.

The brain’s immune response, designed to protect, can become a double-edged sword, making neuroinflammation a critical, yet complex, player in brain health and disease.

What’s the Role of Neuroinflammation In Alzheimer’s disease?

In the context of Alzheimer’s disease (AD), neuroinflammation is not just an ancillary response to the disease’s hallmarks – the tau plaques and neurofibrillary tangles – but rather, it’s a critical player in both the disease’s progression and severity. To understand this, we need to delve into what neuroinflammation actually entails.

At its core, neuroinflammation involves the activation of glial cells – specifically, microglia and astrocytes. These cells are akin to the brain’s own immune system. When they become activated, it’s like sounding an alarm that sets off a cascade of inflammatory processes. This isn’t inherently bad; inflammation is a natural response to damage or pathogens. However, in the case of Alzheimer’s, this process becomes dysregulated.

Microglia, in particular, are central to this. They interact intricately with amyloid-β and tau proteins – the substances that form those characteristic plaques and tangles in Alzheimer’s. When microglia encounter these proteins, they trigger an inflammatory response, releasing a slew of immune mediators. This isn’t a one-off event; it’s a persistent state that contributes significantly to the neurodegeneration seen in Alzheimer’s.

So, what’s the impact of this?

The chronic neuroinflammatory state disrupts various brain functions. It’s like having an overactive immune response that instead of protecting, starts to cause damage, contributing to the neural injury and cognitive decline characteristic of Alzheimer’s.

How does neuroinflammation specifically contribute to Alzheimer’s symptoms?

Here’s a snapshot of research findings linking neuroinflammation and Alzheimer’s symptoms:

• Neuroinflammation is associated with acute and long-term effects, including the risk of dementia and cardiovascular pathology (Satori and Colleagues, 2013).
• Chronic neuroinflammation is thought to directly drive progressive synapse loss and neuronal function decline loss and cognitive decline in conditions such as Alzheimer’s disease (Lecca, et al, 2022).
• Neuroinflammation is considered a pathological hallmark of neurodegenerative diseases and is directly related to cognitive deficits and the neurodegenerative process (Guzzman-Marticnez et al, 2019).
• The immune, physiological, biochemical, and psychological effects of neuroinflammation can interfere with the level of cognition, including memory impairment and cognitive decline (Ahmad et al, 2022).

Overall, neuroinflammation is observed to have far-reaching effects on cognitive function, and its specific impact may vary depending on the underlying condition and the individual. That’s where this study takes off from, investigating the role neuroinflammation has in behavioural changes in people living with Alzheimer’s dementia.

Recent Clinical Studies on Neuroinflammation and Alzheimer’s Disease

Recent clinical studies have highlighted the connection between key Alzheimer’s disease (AD) proteins, amyloid-β (Aβ), and tau, with Neuropsychiatric Symptoms (NPSs). However, neuroinflammation, another significant feature of AD, is gaining attention as an early driver of disease progression.

Microglial activation, a crucial aspect of the brain’s immune response, is suggested to play a pivotal role, not only in AD pathogenesis but also in psychiatric symptoms like psychosis, mania, depression, and anxiety across various conditions. Despite this evidence, it remains unclear whether microglial activation is directly associated with NPS in the AD continuum.

This is where this new study’s findings become interesting.

Let’s explore the nuances of this research to uncover the potential links between neuroinflammation and the psychological manifestations in Alzheimer’s patients.