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Seven reversible causes of dementia in older adults

By: Angela Humbel; Michael Carter, DNSc, DNP, FAAN

Early identification and accurate diagnosis can improve patient outcomes.


  • Some causes of dementia can be reversed through proper identification, intervention, and treatment.
  • Nurses play an essential role in improving the lives of many older adults by recognizing and treating reversible forms of dementia.

As a nurse, you’ll likely care for older adults (65 years and older) who present with memory concerns that may lead you to suspect dementia. However, several medical conditions mimic dementia and can be misdiagnosed as Alzheimer’s disease or a related dementia. These conditions frequently are reversible if diagnosed and treated. An early and accurate diagnosis can reduce the emotional toll on the individual and their caregivers that would result from a misdiagnosis and also save substantial healthcare costs.

In this article, we review seven common reversible causes of dementia and identify their signs and symptoms, diagnostic tests, and treatments. Some dementias can be reversed by resolving the underlying cause, so screening for cognitive impairment is an important first step. (See Screening options.)

Screening options

Screening, which typically takes no more than 10 minutes at a primary care visit, can help identify conditions with symptoms that mimic dementia. Screening tools include:

If screening detects potential cognitive decline, additional evaluation may be warranted to determine the underlying cause. Caregivers or family members can help facilitate the screening process by providing information about changes in the patient’s behavior or memory at home and by comforting the patient during the screening.

1 Hypothyroidism

Hypothyroidism occurs when the thyroid can’t produce enough hormones to meet a person’s metabolic needs. One cause is Hashimoto’s disease, an autoimmune disorder. The less-robust immune response associated with aging puts older adults at increased risk for the disease. Other causes include certain medications that older adults may be taking, such as amiodarone, lithium, rifampin, phenobarbital, phenytoin, and carbamazepine. Hypothyroidism is associated with depression and memory problems related to damage to the brain systems responsible for short-term memory, concentration, and problem-solving. Untreated hypothyroidism also may cause psychosis, anxiety, and somatic complaints. As a result, clinicians may misdiagnose hypothyroidism as an irreversible form of dementia.

Signs and symptoms

Many hypothyroidism symptoms—such as depressed mood, difficulty concentrating, and memory impairment—are nonspecific. The central nervous system is susceptible to changes in thyroid hormone levels, which may slow all cerebral functions, resulting in memory loss and sleepiness. Hypothyroidism also may cause metabolic rate or neurotransmitter synthesis imbalance.

Diagnostic tests

Suspected hypothyroidism is assessed by testing serum thyroid-stimulating hormone (TSH) and thyroxine (T4) levels in the blood. Low T4 or high TSH levels indicate primary hypothyroidism. Treatment should begin as soon as possible to avoid progression to severe hypothyroidism when brain structures may be irreversibly altered.


Hypothyroidism symptoms can be reversed if they’re identified early and thyroid function is restored. Thyroid replacement therapy using levothyroxine reverses most neuropsychological and behavioral abnormalities. (To learn more about hypothyroidism, read “Primary hypo­thyroidism: More common than you think” at

2 Depression

Depression can increase older adults’ risk of developing dementia, and according to Richard and colleagues, symptoms of depression occur in 40% to 50% of those with Alzheimer’s disease or a related dementia. The increased risk for memory impairment is highest in individuals with depression who are 65 and older, more severely depressed, bipolar, or in inpatient treatment settings.

Signs and symptoms

The hippocampus plays a significant role in mood and cognition regulation, which can cause symptoms of cognitive decline. Hippocampal volumes link depression and dementia; reduced volumes are typical in people with mood disorders. People with depression frequently have poor visual and verbal memory, which can result in poor interpretation of information, difficulty processing information, or reduced executive functioning (organizing data and making decisions) on memory tests.

Diagnostic testing

Patients with depression symptoms and memory complaints may be suffering from a brain dysfunction rather than just depression. The way to distinguish brain dysfunction from depression alone is by screening for hippocampal atrophy via magnetic resonance imaging (MRI). In addition, cognitive assessment is performed using screening tools, such as the Mini-Mental State Examination, the AD8 dementia screening interview, and the Mini-Cog. Depression assessment can be accomplished using the Geriatric Depression Scale.


Dementia may be reversed by treating hippocampal atrophy with antidepressant medication in early-onset depression to improve neuron health and prevent neuron damage progression. Patients receiving these medications should be assessed periodically for treatment adherence and symptom improvement.

3 Vitamin B12 deficiency

Memory loss may result from vitamin B12 deficiency (and to a lesser degree, vitamins A, C, and folate deficiencies), mimicking dementia symptoms. According to Wang and colleagues, patients with low vitamin B12 or folate have double the risk of developing Alz­heim­er’s disease, suggesting that they work together for cognitive function.

Signs and symptoms

In addition to memory changes, individuals with vitamin B12 deficiency may present with fatigue, numbness or tingling in hands and feet, vision loss, heart palpitations, GI problems, depression, or behavior changes. Vitamin B12 can affect cognitive function because it’s essential in the structure of myelin, the protective coating of neurons, causing slow neuronal conduction. Vitamin B12 deficiency also may result in transcobalamin deficiency (a disorder that impairs the transport of vitamin B12) and malabsorption and metabolic disorders, which can cause neuronal degeneration. In addition, vitamin B12 or folate deficiency may cause homocysteine levels to rise. Homocysteine has neurotoxic effects that can lead to cell death or neurologic disturbances.

Diagnostic testing and treatment

Patients with recent mental changes should be screened for vitamin B12 deficiency. This condition is reversible with vitamin replacement.

4 Normal pressure hydrocephalus

According to Byrd, approximately 375,000 Americans have been misdiagnosed with dementia or Parkinson’s disease when the underlying condition was normal pressure hydrocephalus (NPH). Misdiagnosis can occur because patients with NPH frequently have word formation difficulty, an inability to carry out simple tasks, or impaired sensory interpretation.

Signs and symptoms

Three distinct areas can be checked to help recognize NPH: cognitive impairment, urinary dysfunction, and mobility impairment (slow and shuffling gait). Early identification of NPH is difficult because symptoms occur gradually. Those that mimic dementia (apathy, dullness in behavior and thinking, and impaired attention) are associated with altered brain structure, and cognitive impairment may be the result of reduced neurotransmitters.

Diagnostic testing

Early detection is critical when NPH is suspected. MRI and cerebrospinal fluid testing are the best ways to accurately diagnose the condition and evaluate its severity.


Treatment for NPH requires surgical placement of a shunt that removes cerebrospinal fluid from the ventricle. Shunt surgery may reverse or improve cognitive impairment if significant dementia hasn’t already de­veloped.

5 Sleep apnea and related deficits

Sleep disturbances, including insomnia and sleep apnea, are common as people age and may lead to reduced cognitive performance, mimicking signs of dementia. Lack of restful sleep can increase the risk of sleep-disordered breathing, decrease total sleep duration, and impair circadian cycles. A study by Hung and colleagues indicates that primary insomnia is associated with a two- to three-fold increased risk for developing dementia.

Sleep apnea is known to cause neuron hypoxia and increase the risk of vascular conditions, such as vascular dementia and stroke, which can increase the risk for dementia. Poor sleep quality and quantity can affect neuron health by interfering with the brain’s natural processes for clearing toxins, which can increase glial cell inflammation and oxidative neurotoxin accumulation. The result can be neuron damage, dementia pathology in the brain, and subsequent dementia-like symptoms.

Diagnostic testing

To determine whether a patient with a sleep disturbance has dementia or depression, their sleep patterns should be assessed with a sleep study. The study will help determine if the patient has obstructive sleep apnea, but it won’t be able to differentiate a sleep disturbance resulting from dementia or depression. These will require complex testing and may still be inconclusive.


Sleep disturbance treatment should begin with basic sleep hygiene strategies and nonpharmacologic approaches, such as transcranial nerve stimulation or cognitive behavioral therapy for chronic insomnia. For patients with sleep apnea, continuous positive airway pressure treatment is essential for improving cell oxygenation, which has been shown by Ferini-Strambi and colleagues to reverse dementia-like symptoms.

6 Alcohol-related dementia

Alcohol-related dementia (ARD) accounts for approximately 10% of early-onset dementia cases. It may result from neurotoxic damage or nutritional deficiencies related to chronic excessive alcohol consumption. For example, thiamine deficiency can lead to Wernicke-Korsakoff syndrome, a neurologic disorder with symptoms that include confusion and cognitive decline.

Signs and symptoms

Signs of ARD include cognitive and behavioral changes, such as impaired orientation, rational functioning, and inhibition. Patients with ARD typically are under the age of 65 years, socially isolated, and male. In addition, their cognitive impairment may be more difficult to detect.

Diagnostic testing

Specific diagnostic criteria for ARD aren’t clear. Frequently, clinicians rely on evaluating changes such as loss of memory or alterations in thinking or reasoning, but only after patients have stopped drinking for some time.


ARD is potentially reversible with timely alcohol use disorder treatment, such as counseling, behavioral therapy, or medication. The earlier ARD is identified, the better the outcome and prognosis for the patient.

7 Medication adverse effects and interactions

Cognitive impairment resulting from prescribed medications is more likely to occur in older than younger adults because they’re already vulnerable to dementia caused by neurodegeneration. Adding a moderately neurotoxic medication might trigger delirium or memory issues.


To definitively identify a medication that’s causing dementia symptoms, the drug causing impairment would have to have been administered before confusion onset and return to normal cognitive baseline would have to occur when the medication is stopped. However, these conditions rarely are met because many older adults take multiple medications. Medicines that can potentiate delirium in adults older than 65 years are found in the American Geriatric Society 2019 Beers Criteria®. These medications—including those with strong anticholinergic properties, conventional and atypical antipsychotics, benzodiazepines, and nonbenzodiazepine and benzodiazepine receptor agonist hypnotics—should be avoided.


Medications causing dementia-like symptoms should be discontinued, as ordered by the provider, while still treating the underlying medical condition. You can educate patients about the risks of taking multiple drugs, work with them to ensure they’re taking only essential medications, and recommend alternative medications when necessary. Always ask patients if they’re taking any over-the-counter medicines, supplements, or natural products, which may adversely interact with prescribed medications. (See Medication considerations.)

Medication considerations

Older adults’ altered metabolism, absorption, and excretion may make them more sensitive to medication adverse effects. However, steps can be taken to mitigate them.

  • A provider may decide that a prescribed medication’s therapeutic effect is more important to the patient’s care plan than potential adverse effects. However, if the adverse effects become too severe, the provider may consider an alternative medication with less potential for harm.
  • Large amounts of free drug can be circulating in an older adult’s system, which can increase the risk of cognitive impairment. To avoid this, medications should be started at the lowest dose and slowly increased until the desired therapeutic effect is reached.
  • Polypharmacy can increase the risk of drug interaction and potential cognitive impairment. Determining which drugs are interacting may be difficult, but providers may consider an alternative medication regimen to address the issue.

Dementia prevention

Nutrition, physical activity, and social networks are critical to dementia prevention. A healthy diet is associated with decreased risk of cardiovascular disease, heart failure, diabetes, and hypertension. For example, in patients with diabetes, elevated blood sugar and insulin resistance can increase the risk of dementia, and more severe conditions (such as hyperglycemic hyperosmolar non-ketonic syn­drome) can deprive neurons of glucose and lead to cognitive impairment.

Physical activity increases circulation, decreases triglycerides and cholesterol, and reduces insulin resistance. Physical activity also can lower blood pressure at rest. Studies, including one by Košcak Tivadar, have shown that exercise slows cognitive decline and reduces the risk of developing dementia.

Increased social contact has been shown to decrease the progress of cognitive decline. Older adults’ social networks may change because of decreased interaction resulting from retirement, children leaving home, and loss of friends or family. Encourage older adults to strengthen their bonds with others and support healthy, social, and therapeutic relationships to maintain healthy mood and neuron health.

Increase your knowledge

Your knowledge of the various causes of reversible dementia, as well as their signs and symptoms, will help you quickly identify them. (See Other causes of reversible dementia.) Providers can then take steps to ensure an accurate diagnosis and make treatment decisions to speed recovery and improve outcomes.

Other causes of reversible dementia

Other causes of reversible dementia include:

  • infections such as HIV and urinary tract infections, which should be ruled out when performing a dementia assessment. Treating the infection may eliminate the dementia symptoms.
  • benign brain tumors that place pressure on the hippocampus, prefrontal cortex, or other brain regions involved in short-term memory. In some cases, the benign tumor can be treated and the cognitive impairment reversed.

Access references at visit

Angela Humbel is an undergraduate bachelor of science in nursing student at The Ohio State University in Columbus. Michael Carter is a distinguished professor emeritus at The University of Tennessee Health Science Center in Memphis. Todd B. Monroe is an associate professor at The Ohio State University.and Todd B. Monroe, PhD, RN-BC, FNAP, FGSA, FAAN


2019 American Geriatrics Society Beers Criteria® Update Expert Panel. American Geriatrics Society 2019 updated Beers Criteria for potentially inappropriate medication use in older adults. J Am Geriatr Soc. 2019;67(4):674-94. doi:10.1111/jgs.15767

Alzheimer’s Association. 2018 Alzheimer’s Disease Facts and Figures.

Bennett S, Thomas AJ. Depression and dementia: Cause, consequence or coincidence? Maturitas. 2014;79(2):184-90. doi:10.1016/j.maturitas.2014.05.009

Byrd C. Normal pressure hydrocephalus: Dementia’s hidden cause. Nurse Pract. 2006;31(7):36-7. doi:10.1097/00006205-200607000-00006

Cheng C, Huang C-L, Tsai C-J, Chou P-H, Lin C-C, Chang C-K. Alcohol-related dementia: A systemic review of epidemiological studies. Psychosomatics. 2017;58(4):331-42. doi:10.1016/j.psym.2017.02.012

Ferini-Strambi L, Baietto C; Di Gioia MR, et al. Cognitive dysfunction in patients with obstructive sleep apnea (OSA): Partial reversibility after continuous positive airway pressure (CPAP). Brain Res Bull. 2003;61(1):87-92. doi:10.1016/s0361-9230(03)00068-6

Folstein MF, Folstein SE, McHugh PR. “Mini-mental state.” A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res. 1975;12(3):189-98. doi:10.1016/0022-3956(75)90026-6

Galvin JE, Roe CM, Powlishta KK, et al. The AD8: A brief informant interview to detect dementia. Neurology. 2005;65(4):559-64. doi:10.1212/01.wnl.0000172958.95282.2a

Holwerda TJ, Deeg DJH, Beekman ATF, et al. Feelings of loneliness, but not social isolation, predict dementia onset: Results from the Amsterdam Study of the Elderly (AMSTEL). J Neurol Neurosurg Psychiatry. 2014;85(2):135-42. doi:10.1136/jnnp-2012-302755

Hong S, Banks WA. Role of the immune system in HIV-associated neuroinflammation and neurocognitive implications. Brain Behav Immun. 2015;45:1-12. doi:10.1016/j.bbi.2014.10.008

Hung CM, Li YC, Chen HJ, et al. Risk of dementia in patients with primary insomnia: A nationwide population-based case-control study. BMC Psychiatry. 2018;18(1):38. doi:10.1186/s12888-018-1623-0

Koščak Tivadar B. Physical activity improves cognition: Possible explanations. Biogerontology. 2017;18(4):477-83. doi:10.1007/s10522-017-9708-6

Mander BA, Winer JR, Jagust WJ, Walker MP. Sleep: A novel mechanistic pathway, biomarker, and treatment target in the pathology of Alzheimer’s disease? Trends Neurosci. 2016;39(8):552-66. doi:10.1016/j.tins.2016.05.002

Moise D, Madhusoodanan S. Psychiatric symptoms associated with brain tumors: A clinical enigma. CNS Spectr. 2019;11(1):28-31. doi:10.1017/s1092852900024135

Monroe T, Carter M. Using the Folstein Mini Mental State Exam (MMSE) to explore methodological issues in cognitive aging research. Eur J Ageing. 2012;9(3):265-74. doi:10.1007/s10433-012-0234-8

Monroe T, Carter M, Parish A. A case study using the Beers List criteria to compare prescribing by family practitioners and geriatric specialists in a rural nursing home. Geriatr Nurs. 2011;32(5):350-6. doi:10.1016/j.gerinurse.2011.07.003

Ninomiya T. Epidemiological Evidence of the Relationship Between Diabetes and Dementia. Adv Exp Med Biol. 2019;1128:13-25. doi:10.1007/978-981-13-3540-2_2

Oliveira LM, Nitrini R, Román GC. Normal pressure hydrocephalus: A critical review. Dement Neuropsychol. 2019;13(2):133-43. doi:10.1590/1980-57642018dn13-020001

Richard E, Reitz C, Honig LH, et al. Late-life depression, mild cognitive impairment and dementia. JAMA Neurol. 2013;70(3):374-82. doi:10.1001/jamaneurol.2013.603

Spence JD. Metabolic vitamin B12 deficiency: A missed opportunity to prevent dementia and stroke. Nutr Res. 2016;36(2):109-16. doi:10.1016/j.nutres.2015.10.003

Steenland NK, Auman CM, Patel PM, et al. Development of a rapid screening instrument for mild cognitive impairment and undiagnosed dementia. J Alzheimers Dis. 2008;15(3):419-27.

Troussière A-C, Charley CM, Salleron J, et al. Treatment of sleep apnoea syndrome decreases cognitive decline in patients with Alzheimer’s disease. J Neurol Neurosurg Psychiatry. 2014;85(12):1405-8. doi:10.1136/jnnp-2013-307544

Wändell P, Carlsson AC, Sundquist J, Sundquist K. Effect of levothyroxine treatment on incident dementia in adults with atrial fibrillation and hypothyroidism. Clin Drug Investig. 2019;39(2):187-95. doi:10.1007/s40261-018-0740-3 

Wang HX, Wahlin A, Basun H, Fastbom J, Winblad B, Fratiglioni L. Vitamin B(12) and folate in relation to the development of Alzheimer’s disease. Neurology. 2001;56(9):1188-94. doi:10.1212/wnl.56.9.1188

2 Comments. Leave new

  • We have to give a try on herbal supplements which effectively get rid of herbal ALS condition dramatically. After 15 weeks of her usage,she lost touch with reality. Suspecting it was the medication I took her off the riluzole (with the doctor’s knowledge) and started her on the ALS natural herbal formula we ordered. It is advisable to always try natural herbs at first because www neutralizes her ALS/MND which surprises everyone at home.

    • This article mentions test’g of TSH & T4 re Hypothyroidism, that if T4 is low… How low is low, under what number wld be considered too low.
      Thanks for any response you can offer.


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