Parkinson’s disease is a progressive neurodegenerative disease that is most commonly known for affecting movement. It primarily impacts dopaminergic, or dopamine-producing, neurons in a specific area of the brain known as the substantia nigra.

Typically, symptoms develop slowly over years and continue to worsen as the disease progresses. While the manifestation of symptoms tends to vary from patient to patient, individuals with Parkinson’s disease will likely experience a combination of cognitive impairments (how they think) and functional impairments (how they move) throughout the disease course.

Below, we provide a list of the most common signs of Parkinson’s disease, including both motor and non-motor symptoms.

Signs of Parkinson’s Disease

When most people think of Parkinson’s disease, they think of symptoms like tremors and changes in gait. While Parkinson’s disease is most known for causing motor symptoms, it can also cause non-motor symptoms, such as cognitive dysfunction and autonomic dysfunction. 

Motor-Related Signs of Parkinson’s Disease

• Resting tremor: A tremor, or slight shaking, of the hand, fingers, or chin while at rest is a very common sign of Parkinson’s disease. Some individuals with Parkinson’s will rub their thumb and forefinger back and forth; this is known as a pill-rolling tremor.
• Bradykinesia (slowed movement): As the disease progresses, movement can become slow, making simple activities challenging and time-consuming. This can include a reduction in automatic movements (such as swinging the arms when walking or blinking), a general slowness in physical actions, or a mask-like facial expression (decreased expression on the face).
• Rigidity: Alongside resting tremor and bradykinesia, stiffness and rigidity in the muscles of the limbs are some of the most common symptoms of Parkinson’s disease. Bradykinesia and rigidity often contribute to more frequent falls. 
• Changes in posture, balance, or gait: Gait is a person’s pattern of walking. Bradykinesia and unstable posture can both contribute to difficulties with walking, particularly as the disease progresses. When walking, steps can become small, the patient’s feet may drag, or they may walk with a shuffle. 
• Changes in speech: Patients with Parkinson’s disease often experience changes in speech, including soft or faint speaking volume, changes in speaking speed, slurring of words, or monotone speech.
• Changes in writing: Particularly in the later stages, writing can become challenging. Handwriting may become small or cramped.

Non-Motor-Related Signs of Parkinson’s Disease

• Changes in cognitive function: Changes in cognitive functions, such as memory and thinking, can vary widely, ranging from minor difficulties with concentrating or multitasking to more significant changes that interfere with the ability to complete normal day-to-day activities and tasks (Activities of Daily Living).
• Loss of automatic functions: Parkinson’s disease often affects automatic/involuntary functions performed by the body. This can cause constipation, urination problems, excessive sweating, low blood pressure, and sexual problems.
• Anxiety and depression: Mood disturbances, such as depression and anxiety, are common in Parkinson’s disease, particularly in the very early stages.
• Reduced sense of smell: Loss or reduction of smell (anosmia) is one of the earliest reported symptoms and is quite common in Parkinson’s disease, with up to 95% of Parkinson’s patients experiencing it to some degree. 
• Dizziness or fainting: Feeling lightheaded or dizzy upon standing due to orthostatic hypertension is a common symptom of Parkinson’s disease and is caused by a dip in blood pressure.
• Sleeping troubles: Sleep and brain health are closely linked. Sleeping issues are common in neurodegenerative diseases and can occur very early in the disease course. Patients may have difficulty falling asleep or staying asleep, thrash around while sleeping, experience daytime sleepiness, or have very vivid dreams.

Previous research surrounding kidney disease and dementia demonstrated mixed and often conflicting results regarding the relationship between kidney function and the rate of dementia diagnosis. However, more recently, a study designed to evaluate the entire spectrum of kidney function and larger sample sizes indicated a strong relationship.

Below, we take a deep dive into this study, discussing how it compares to previous research surrounding kidney disease and dementia risk and how to address the limitations of current research. 

Kidney Disease and Dementia Risk

According to a five-year study of a health care use cohort published in Neurology in May of 2021, both lower kidney function and steeper kidney function decline are associated with the development of dementia in older adults (≥65 years of age).

Study Design, Outcome Measures, and Results

Because community-based reports surrounding the link between the estimated glomerular filtration rate (eGFR) and dementia risk have shown conflicting results, this study aimed to investigate on a large scale the connections between kidney function, kidney function decline, and dementia incidence. 

eGFR is commonly used in clinical practice to assess kidney function, as this calculation can indicate how well the kidneys are filtering out specific agents produced by the body, such as creatinine and cystatin C.

The study utilized data from the Stockholm Creatinine Measurements (SCREAM) project, which included data from all residents receiving serum creatinine tests between the years 2006 and 2011. This enabled the researchers to analyze more than 90% of the total census population of individuals aged 65 and over (329,822 individuals). Exclusion criteria included any recorded history of dementia, missing information regarding age or sex, and undergoing kidney replacement therapy at cohort entry. 

Study Outcome Measures:

• Primary Outcome: The first recorded diagnosis of all-cause dementia or the initiation of dementia treatment drugs
• Secondary Outcome: The first recorded diagnosis of Alzheimer’s disease-related dementia and vascular dementia

The primary findings of this study were as follows:

• Over a median follow-up of five years, 18,983 cases of dementia were detected.
• Dementia incidence rates were significantly higher with lower eGFR: From 6.56/1,000 person-years in those with eGFR of 90 to 104 mL/min to 30.28/1,000 person-years in those with eGFR <30 mL/min.
• After multivariable adjustment, lower eGFR was associated with a higher dementia risk ((hazard ratio [HR] 1.71, 95% confidence interval [CI] 1.54–1.91 in eGFR 30–59 mL/min; HR 2.62, 95% CI 1.91–3.58 in eGFR <30 mL/min) compared with eGFR of 90 to 104 mL/min).
• A steeper decline in eGFR (decline >2 mL/min/1.73 m³/y) within one year was associated with a higher dementia risk.
• Risk magnitudes were stronger for vascular dementia than for Alzheimer’s disease-related dementia.
• As many as 10% (95% CI 6%–14%) of dementia cases could be attributed to eGFR <60 mL/min/1.73 m³. 

A Comparison With Previous Research Surrounding Kidney Disease and Dementia Risk

Previous studies investigating kidney disease and dementia risk have had mixed findings, with some aligning with the results in the above study and others demonstrating conflicting findings.

For example, a Japanese study published in 2018 that analyzed 1,562 participants ≥60 years of age also observed a higher dementia risk in individuals with eGFR <60 mL/min. On the other hand, studies such as this French population-based Three-City study did not show increased dementia risks for individuals with eGFR <60 mL/min. However, these studies did find that the stratum of eGFR of 45 to 60 mL/min was associated with an increased incidence of vascular dementia.

The discrepancy between the findings may very well be due to the differing study designs and outcome measures. While some study designs involved screening, others involved health care extraction. Similarly, while some study outcome measures involved neuropsychological performance, others related to dementia diagnosis and/or drug dispensations. 

For example, utilizing outcome measures such as scores from traditional neuropsychological assessments (e.g. the Mini-Mental State Exam) may not produce results granular enough to truly understand neurocognitive function and dementia risk. These assessments frequently produce noisy, highly variable results that lack the specificity and granularity to confidently draw conclusions on true neurocognitive function, let alone place them on a disease continuum.

Future studies surrounding kidney disease and dementia risk will likely require more robust outcome measures, assessing a breadth of neurocognitive domains at a highly detailed level. Future studies may also include higher frequency neurocognitive testing to better understand changes in neurocognitive function over time to enable researchers to create more robust associations between kidney function and dementia risk.

It is no secret that glucose, a form of sugar, is the main source of energy for every cell in our bodies, including our brain cells. Because the brain is packed with neurons, it uses more energy than any other organ in the body. 

Our brains reward us for consuming sugar. Whether you are eating a delicious meal, sharing a kiss with someone you love, or enjoying a sugary treat, the mesolimbic dopamine system activates, releasing dopamine (a feel-good brain chemical) and reinforcing that behavior.

While our brains depend on sugar to function properly, too much of this fuel can be detrimental to brain health. Below, we break down how sugar impacts the brain, including its effect on cognitive function, mood, and disease risk.

How Sugar Impacts the Brain

Even if you don't have a sweet tooth, you might be consuming significantly more sugar than you think, particularly if your diet includes a lot of processed foods. Sugar is one of the most common ingredients in processed foods. The average American adult, teenager, and child consume about 17 teaspoons of added sugar per day, which is well over the amount recommended by the American Heart Association—no more than 6 teaspoons (25 grams) and 9 teaspoons (36 grams) per day for most adult women and men, respectively.

With that in mind, let’s take a look at how sugar impacts the brain.

How Sugar Impacts Cognitive Function

Brain functions, such as thinking, memory, and learning, are closely linked to glucose levels. When glucose levels are low, such as with hypoglycemia, the lack of energy for brain function can cause poor cognitive function. When glucose levels are high over a prolonged period, such as with diabetes, the brain’s functional connectivity is affected, and the brain volume can reduce (atrophy). High blood glucose levels can also damage blood vessels in the brain, restricting blood flow. This restricted blood flow can cause cognitive impairment or even lead to the development of vascular dementia.

A 2016 study found that high sugar consumption may cause neuroinflammation (inflammation in the brain) in regions of the brain that are crucial for memory. A 2017 study found that a higher intake of sugary beverages was associated with lower total brain volume and poorer performance on tests of episodic memory. They also found that daily fruit juice intake was associated with lower total brain volume, hippocampal volume, and poorer episodic memory. This implies that excess sugar consumption was associated cross-sectionally with markers of preclinical Alzheimer’s disease.

How Sugar Impacts Mood

While sugar consumption may boost your mood momentarily, high sugar consumption has been linked to poor emotional regulation and an increased risk of mental health problems. As we mentioned before, sugar consumption affects the mesolimbic dopamine system. Because this system influences emotion and behavior, sugar consumption can impact our mental health and behavior.

A 2017 study of 23,245 individuals found that men who consumed the most sugar were 23% more likely to be diagnosed with a mental disorder after five years compared to those who consumed the least sugar.

High-Sugar Diets and Disease Risk

High-sugar diets have long been associated with health problems such as diabetes, heart disease, and obesity. However, many people don’t know that these conditions are also risk factors for Alzheimer’s disease and other causes of dementia. Research suggests that a high-fat, high-sugar diet is associated with greater risk and earlier onset of Alzheimer’s disease, whereas a low-sugar diet high in unsaturated fats, fiber, and protein is associated with lower rates of Alzheimer’s disease.

Everything in Moderation: Tips for Better Brain Health

Like most things, sugar can be okay in moderation. We all deserve a sweet treat every now and again, but we should also be observant and mindful of what we are putting into our bodies. Here are some helpful tips to help manage your sugar intake:

• Opt for whole, natural foods: Processed foods are often very high in sugar, salt, and fat. If you are craving something sweet, consider a handful of berries instead. Of course, berries will have natural sugars, but what you want to watch out for is added sugars.
• Read the nutrition label: There are many different names for sugar you will come across when reading a nutrition label. Some of the most common ones include fructose, dextrose, sucrose, corn syrup, and honey. 
• Swap out the sugary drinks: Sodas, juices, and other sweet drinks contain an alarming amount of sugar. A single 12-ounce can of Coke contains 39 grams of sugar—more than the daily recommended amount of sugar for both men and women. 
• Cut the serving back or make substitutions: If you are making baked goods, try cutting back the amount of sugar you add by a third or a half. You can also swap out granulated sugar with foods like unsweetened applesauce.

Aside from cutting down your sugar intake, there is plenty you can do to maintain a healthy brain, including:

• Quitting smoking.
• Daily exercise (30-60 minutes/day).
• Eating a heart-healthy diet.
• Getting adequate sleep.
• Minimizing stress.
• Controlling alcohol consumption.

It is never too early—or too late—to make changes to your lifestyle and understand and monitor your brain health.

According to the Alzheimer’s Association, more than six million Americans are living with Alzheimer’s disease as of 2022; by 2050, this number is projected to rise to nearly 13 million. In 2022, Alzheimer’s disease and other causes of dementia will cost the nation $321 billion; by 2050, these costs could reach nearly $1 trillion.

The increasingly high prevalence and the consequent social and economic impact of Alzheimer’s disease demonstrate the importance of research efforts surrounding modifiable risk factors and Alzheimer's prevention strategies.

Recently, researchers have uncovered a connection between circadian rhythm and Alzheimer's disease. Below, we take a closer look into research surrounding this relationship and discuss sleep disturbances as an emerging target for Alzheimer’s disease prevention.

The Relationship Between Circadian Rhythm and Alzheimer’s Disease

Circadian rhythm is the natural cycle of physical, mental, and behavioral changes that our bodies go through in a 24-hour cycle. Circadian rhythms can affect sleep-wake cycles, hormonal activity, body temperature, eating and digestion, and other functions. You can think of this as part of your biological clock that helps you fall asleep at night and wake up in the morning. 

It is widely known that sleep-wake and circadian rhythm disruption is common in Alzheimer’s disease patients—these changes occur early in the disease course and may even precede the development of cognitive symptoms. However, increasing evidence suggests that these disturbances may also contribute to the development and progression of Alzheimer’s and other neurodegenerative diseases. 

Research Linking Circadian Rhythm and Alzheimer’s Disease

The etiopathogenesis of circadian rhythm disturbances and Alzheimer’s disease share several features that suggest they may be a mutually dependent pathway. Pathological mechanisms, such as amyloid production and clearance, neuroinflammation, and oxidative stress, can be linked to circadian rhythm disruption, sleep deprivation, and Alzheimer’s disease. Here is what research tells us about the connection between circadian rhythm and Alzheimer’s disease:

• Sleep-wake cycles regulate Alzheimer’s disease pathology: Many studies have shown that sleep-wake cycles may regulate the level of beta-amyloid proteins—one of the primary neuropathological hallmarks of Alzheimer’s disease. Clearance of this protein is essential for a healthy neuronal microenvironment. The accumulation of this protein (known as beta-amyloid plaques) is believed to accelerate the development and progression of Alzheimer’s disease. A 2022 study demonstrated that the immune cells responsible for clearing this protein from the brain follow a 24-hour circadian oscillation. This suggests that disruptions in the circadian rhythm may affect the clearance of these harmful plaques, and, consequently, the accumulation of beta-amyloid.
• Sleep deprivation exacerbates Alzheimer’s pathology: A 2022 study found that chronic fragmentation of the sleep-wake rhythms increased hippocampal beta-amyloid levels and neuroinflammation in Alzheimer's disease mouse models. These findings suggest disruption of daily-sleep wake cycles may increase the risk of developing Alzheimer’s disease. Similar findings have been demonstrated in human studies. In a small study of humans, researchers found that just one night of sleep deprivation resulted in a significant increase in beta-amyloid burden in the right hippocampus and thalamus.
• Insufficient sleep may increase dementia risk: In a 2021 study, researchers at Harvard Medical School found that those who slept fewer than five hours per night were twice as likely to develop dementia compared to those who slept six to eight hours per night. 
• Sleep disturbances may accelerate neurodegeneration: In addition to contributing to beta-amyloid pathology, animal models of neurological diseases, such as Alzheimer's, suggest that chronic sleep insufficiency may accelerate the neurodegenerative process.

When taken as a whole, this research suggests that sleep and Alzheimer’s disease share a complex bidirectional relationship. While more research is needed to better understand this relationship, circadian rhythm and sleep-wake cycles may be ideal targets for potential interventions to slow the progression of Alzheimer’s disease and possibly even prevent its development.

Sleep Disturbance as a Modifiable Risk Factor for Alzheimer's Disease

In light of research surrounding circadian rhythm and Alzheimer's disease, the circadian rhythm has emerged as an interesting target for Alzheimer’s disease prevention. Therapy-based interventions, such as bright light therapy, can be utilized to regulate the circadian rhythm by gradually shifting sleeping patterns back to a “normal” sleep-wake pattern, thus reducing sleep-wake disturbances. This may aid in reducing the risk of developing Alzheimer’s disease in those with circadian dysfunction and may help slow the progression of the disease for those diagnosed with Alzheimer’s disease.

Aside from getting sufficient sleep, other Alzheimer's prevention strategies include:

• Quitting smoking.
• Exercising daily (30-60 minutes per day).
• Eating a heart-healthy diet.
• Minimizing stress.
• Controlling alcohol consumption.
• Increasing mental and social engagement.

The growing amount of research surrounding modifiable risk factors emphasizes the need to monitor the brain health of individuals with risk factors for Alzheimer's disease, including circadian rhythm and sleep-wake disorders. The brain health of all individuals who have known risk factors, whether modifiable or nonmodifiable, should be assessed and monitored early and frequently to detect neurocognitive changes as early as possible. Early detection of Alzheimer’s disease is crucial, as it can enable early intervention and, consequently, better health outcomes. 

Primary care practitioners are often the first to address a patient’s or family’s concerns about memory loss or the possibility of dementia. Detecting cognitive decline as early as possible is fundamental to a patient’s ability to receive earlier access to treatments and therapies, and, consequently, more effective treatment and improved health outcomes.

There are several assessments available to measure cognitive decline—each with its own strengths and shortcomings. Below, we provide guidance on how to measure cognitive decline in older patients, including general information on how cognitive testing works, an overview of common cognitive assessment tools, and the strengths and limitations of such assessments.

What Is Cognitive Testing?

Cognitive testing is often used by healthcare providers to detect changes in cognitive function and screen for Mild Cognitive Impairment. Of course, it is important to understand that not all changes in cognitive function are indicative of the presence of Alzheimer’s or other causes of dementia. It is possible to have cognitive changes, such as memory loss, but not dementia. 

Cognitive tests typically assess aspects of cognition such as those listed below:

• Memory 
• Orientation
• Attention
• Visuospatial abilities
• Language 
• Judgment
• Ability to learn new things

There are several types of cognitive assessments, but generally, these assessments will require the patient to answer a series of questions and/or complete simple tasks.

How To Measure Cognitive Decline in Older Patients

To measure a decline in cognitive function, it is necessary to regularly and frequently assess brain function over time. By tracking trends and patterns in assessment scores longitudinally, changes in cognition can be identified.

Three of the most common tools utilized to measure cognitive decline are the Mini-Mental State Examination (MMSE), the Montreal Cognitive Assessment (MoCA), the Mini-Cog, and the general practitioner assessment of cognition (GPCOG). Here is a look at how each of these assessments works.

MMSE

The MMSE is scored on a 30-point scale and takes roughly five to 10 minutes to administer. This assessment asks the patient to state the current date, count backward, and identify everyday objects. 

According to the Alzheimer’s Association, score ranges on both the MMSE and the MoCA may indicate the following:

• Mild dementia: score of 20-24
• Severe dementia: score of 13-20

MoCA

The MoCA, also scored on a 30-point scale, takes 10 to 15 minutes to administer and includes the same aspects of the MMSE, with the addition of the following two tasks:

• The Clock Drawing Test (CDT): The patient is tasked with drawing a clock, placing the numbers in their proper locations, then “setting” the clock to a specific time.
• The Trail Making Test: In this two-part test, the patient must first connect 25 numbered circles, starting with one and ending at 25, as quickly as possible while maintaining accuracy. In the next part of the test, the patient must connect 25 numbered and lettered circles, alternating between numbers and letters. In other words, the path is to be traced following the pattern “1-A-2-B-3-C-4-D” and so on.

Mini-Cog

The Mini-Cog takes roughly three minutes to complete. This test consists of three steps:

1. The patient is asked to remember three words.
2. The patient completes the CDT.
3. The patient must then recall and state the three words from before the CDT. 

The patient receives up to three points for word recall and up to two points on the CDT, with a maximum score of five points. A score of three, four, or five indicates a lower likelihood of dementia but does not rule out cognitive impairment. 

GPCOG

The GPCOG is another screening tool used to measure cognitive decline and takes between two and five minutes to administer. It is separated into two steps, with the first step being scored on a nine-point scale and the second step being scored on a six-point scale.

Step One:

Step one of the GPCOG includes five tasks:

1. The patient is asked to remember a name and address to recall at a later time (in task five).
2. The patient is asked to state the date.
3. The patient completes the CDT.
4. The patient is asked to talk about something that has happened in the news recently.
5. The patient is tasked with recalling the name and address from task one.

If the patient scores nine, this means no significant cognitive impairment is indicated and no further testing is necessary. If the patient scores between five and eight, testing proceeds to step two. If the patient scores between zero and four, cognitive impairment is indicated.

Step Two:

In step two, the patient’s informant is asked a series of questions about the patient’s day-to-day function compared to a few years ago. If the patient scores between zero and three, cognitive impairment is indicated.

*Note: While the administration time for the above assessments may be brief, the clinical waiting time—as well as the analysis and results reporting time—can make this process rather inefficient.

Advantages and Limitations of Cognitive Assessment Tools

Each of the assessments above has its unique strengths and shortcomings regarding the thoroughness, accuracy, and validity of the assessment design. According to the Alzheimer’s Association, these are the key advantages and limitations of each assessment:

Cognitive Assessment Tool	Advantages	Limitations
MMSE	Most widely used and studied worldwide Often used as reference for comparative evaluations of other assessments Required for some drug insurance reimbursements	Education, age, language, and cultural bias Highly educated, yet still cognitively impaired, subjects may pass this assessment (the ceiling effect) Proprietary Best performance for at least moderate cognitive impairment
MoCA	Designed to test for Mild Cognitive Impairment Accessible in multiple languages Tests many separate domains	Lack of studies in general practice settings Education bias (≤12 years) Limited use and evidence due to published data being relatively new
Mini-Cog	Developed for and validated in primary care and multiple languages and cultures Little or no education/language/race bias Short administration time	Use of different word lists may affect failure rates Some study results based on longer tests with the Mini-Cog elements are reviewed independently
GPCOG	Developed for and validated in primary care Little or no education bias Accessible in multiple languages	Patient component scoring has indeterminate range that requires an informant score to assess as pass or fail Lacks data on any language and cultural biases

Addressing the Limitations of Traditional Cognitive Assessment Tools

Many of the above assessments are purely cognitive batteries that only assess a small subset of neurocognitive domains. These assessments are not ecologically valid, meaning the design of the evaluation does not align with neurocognitive states representative of Activities of Daily Living (ADLs). Because of these limitations, such assessments often produce noisy, highly variable results that lack the specificity and granularity to adequately measure cognitive function and track cognitive decline over time.

As we get older, it is normal to be concerned about experiencing changes in memory or developing Alzheimer’s disease-related dementia. Maybe you are concerned about forgetting to pay a bill every once in a while or about forgetting a birthday on occasion. It is important to understand that there are many potential causes of memory loss; it is possible to have memory loss but not dementia.

Below, we provide information on signs of memory loss, potential causes of memory loss that are not dementia, how Alzheimer's disease causes memory loss, and how to distinguish between normal cognitive aging and dementia.

Signs of Memory Loss

Memory loss is one of the most recognizable early signs of dementia. Memory loss that is severe enough to disrupt daily living may be a symptom of Alzheimer’s disease or other causes of dementia. Here are six common signs of memory loss:

1. Repeatedly asking the same questions
2. Forgetting common words or mixing up words
3. Struggling to follow a list of instructions or steps required to complete familiar tasks
4. Becoming lost in familiar areas or places
5. Difficulty understanding time or place
6. Misplacing items in inappropriate places or losing things frequently

Memory Loss But Not Dementia: Other Potential Causes

Dementia is an umbrella term used to describe a decline in cognitive abilities that interfere with an individual’s ability to complete basic day-to-day activities, or Activities of Daily Living. Dementia is not a specific disease but rather describes a group of symptoms—one of which is memory loss. Alzheimer’s disease, on the other hand, is the most common cause of dementia. In other words, Alzheimer’s disease is a specific disease that causes Alzheimer’s-related dementia. Similarly, Parkinson’s disease is a specific disease that causes Parkinson’s disease-related dementia (also called Parkinson’s disease dementia).

Memory loss is not unique to dementia—several medical conditions can cause memory loss and other cognitive changes. Conditions that can cause changes in memory include:

• Head injury.
• Some thyroid, liver, and kidney disorders.
• Anxiety and depression.
• Functional cognitive disorder (FCD).
• Vitamin deficiencies.
• Blood or infections in the brain.

How Alzheimer’s Disease Causes Memory Loss

Loss of memory is among the first symptoms commonly reported by patients with Alzheimer’s disease. The primary underlying cause of memory loss, confusion, and forgetfulness in Alzheimer’s disease patients is the progressive damage caused by Alzheimer’s. This progressive damage is thought to be largely due to Alzheimer’s pathology—namely beta-amyloid plaques and neurofibrillary tangles. The unique patterns or characteristics of impaired memory functions in Alzheimer's disease patients depend on where an Alzheimer’s patient lies on the disease continuum, meaning what stage of the disease the patient is in. 

Memory Loss But Not Dementia: Distinguishing Between Normal Cognitive Aging and Dementia

As we age, changes occur in all parts of the body, including the brain. For normal aging, cognitive abilities, such as memory, are likely to decline very slowly and gradually over time, with only a minor decline in cognitive function. For Alzheimer’s disease-related dementia, this decline in cognitive abilities follows a much steeper curve. A newer school of thought within the field of neurology is that Alzheimer’s disease-related dementia is just accelerated aging of the brain, meaning this decline occurs at an accelerated rate compared to cognitively healthy individuals.

Some changes to memory skills and other cognitive abilities as you age are normal. Minor changes to abilities such as memory, planning, organizing, and decision-making can occur with normal, healthy cognitive aging. For example, you may experience:

• Taking slightly longer than before to learn new things.
• Forgetting to pay a bill every once in a while.
• Minor decreases in your ability to pay attention.
• Being slower to find the right word to use.
• Having mild difficulty with multitasking.

For individuals with dementia, cognitive impairments will likely be more severe, enough to interfere with Activities of Daily Living. Changes beyond memory loss that may indicate the presence of Alzheimer’s disease-related dementia may include a decline in cognition in domains such as cognitive processing speed and executive function and a decline in function in domains such as motor function, gait, speech and articulation, and vision and eye movement.

If you have concerns about memory loss or other changes in cognitive abilities, your doctor will likely want to rule out any other potential causes of memory loss and may test you for Alzheimer’s disease. 

Why is it that whenever we are feeling down or are having a bad day, we are often told to go for a walk to get some fresh air? From taking a stroll through your local park to taking in the scenery on a hike in the mountains, being outside in nature can be restorative and grounding.

How and where we spend our time plays a huge role in our overall health and wellbeing, including our mental and cognitive health. An emerging body of research suggests that being in nature, or even viewing scenes of nature, can reduce stress, fear, and anger, increase pleasant feelings, and even sharpen some of our cognitive abilities.

Below, we take a closer look at nature’s effect on the brain, including potential physiological and cognitive benefits of exposure to nature, the use of nature for therapy-based interventions, and the best way to stay in touch with your brain health.

Nurtured by Nature: Understanding Nature’s Effect on the Brain

There are so many factors that impact our mental and cognitive health that we don’t often think about. Researchers and healthcare professionals alike are increasingly recognizing the immense impact social and environmental factors have on our health. Experts estimate that only 10% of longevity can be attributed to healthcare services and only 30% to genetics, while 60% can be attributed to individual behaviors and social and environmental factors.

Nature’s Effect on the Brain: Potential Physiological and Cognitive Benefits

With this new understanding, researchers have begun investigating how specific interactions and behaviors, such as spending time in nature, affect brain health. Emerging research suggests that experiencing or viewing nature may provide potential benefits such as:

• Reduced stress, anger, and fear.
• Increased feelings of kindness, generosity, and trust.
• Reduced risk of developing psychiatric disorders.
• Improved working memory.
• Improved short-term memory.

Here is a closer look at some of the research surrounding nature’s effect on the brain:

• In a series of studies published in 2014, researchers analyzed the impact of nature on the willingness of participants to be generous, trusting, and helpful towards others. They found that after being exposed to the “more beautiful” nature scenes, participants acted more generously and were more trusting of others. 
• A 2015 study aimed to investigate the impact of nature experience on affect and cognition, with 60 participants randomly assigned to walk 50 minutes in either a natural or urban environment while completing a series of cognitive and psychological assessments before and after their walk. The researchers found that compared to the urban walk, the nature walk produced affective benefits, such as reduced anxiety, rumination, and negative affect and preservation of positive affect, as well as cognitive benefits, such as improved working memory performance. 
• A 2018 study assessing the effect of exposure to biophilic indoor environments on physiological and cognitive performance found that biophilic environments decrease negative emotions, increase positive emotions, and improve short-term memory by 14%.
• A 2019 nationwide study assessed the association between urban living (with lower levels of green space) and the risk of developing psychiatric disorders, such as depression, bipolar disorder, schizophrenia, eating disorders, and substance abuse. They found that children who grew up in the lowest levels of green space had up to a 55% higher risk of developing a psychiatric disorder independent from the effects of other known risk factors. This suggests that the prolonged presence of green space may be important for mental health.
• Many studies have found that even viewing images or videos of nature can improve emotional well-being. A 2020 case study assessed the effects of combining nature therapy and music therapy for dementia patients. They found that after the combined visual and auditory experience, the tranquility levels of memory care residents improved significantly compared to baseline.

While more research is needed to truly understand nature’s effect on the brain and the mechanisms at work, increasing scientific evidence suggests that viewing elements of nature is associated with physiological relaxation.

Nature as Therapy

In recent years, nature therapy, or ecotherapy, has been proposed as a novel form of therapy for stress recovery and health promotion. Nature therapy is defined as “a set of practices aimed at achieving ‘preventive medical effects’ through exposure to natural stimuli that render a state of physiological relaxation and boost the weakened immune function to prevent disease.” 

When paired with other elements of healthy living, such as eating a healthy diet, exercising regularly, and getting enough sleep, exposure to nature may be utilized to prevent or mitigate risk factors for conditions such as dementia and mood disorders. Nature therapy is also being investigated as a means to treat or alleviate behavioral and psychological symptoms of dementia (BPSD).

Staying in Touch with Your Brain Health with Altoida

Brain health is essential to everything we do daily and plays an important role in our ability to live long, healthy, and happy lives. Understanding how our actions and lifestyles impact our brains allows us to take charge of our overall wellness by incorporating elements of healthy living and regularly monitoring our brain health.